peptic ulcer

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PEPTIC ULCER:

PEPTIC ULCER

Definitions:

Definitions Ulcer: A lesion on an epithelial surface (skin or mucous membrane) caused by superficial loss of tissue Erosion: A lesion on an epithelial surface (skin or mucous membrane) caused by superficial loss of tissue, limited to the mucosa

Definitions:

Definitions Peptic Ulcer An ulcer of the alimentary tract mucosa, usually in the stomach or duodenum, & rarely in the lower esophagus, where the mucosa is exposed to the acid gastric secretion It has to be deep enough to penetrate the muscularis mucosa

Peptic Ulcer Disease:

Peptic Ulcer Disease

Gastric Mucosa & Secretions:

Gastric Mucosa & Secretions The inside of the stomach is bathed in about 2 liters of gastric juice every day Gastric juice is composed of digestive enzymes & concentrated hydrochloric acid, which can readily tear apart the toughest food or microorganism The gastroduodenal mucosal integrity is determined by protective ( defensive ) & damaging ( aggressive ) factors

Gastric Mucosa & Secretions:

Gastric Mucosa & Secretions The Defensive Forces Bicarbonate Mucus layer Mucosal blood flow Prostaglandins Growth factors The Aggressive Forces Helicobacter pylori HCl acid Pepsins NSAIDs Bile acids Ischemia and hypoxia. Smoking and alcohol When the aggressive factors increase or the defensive factors decrease, mucosal damage will result, leading to erosions & ulcerations

Because of Imbalance:

Because of Imbalance Imbalance primarily between Aggressive factors and Defensive factors: Aggressive factors, e,g, acid, pepsin, bile etc. Defensive factors, e.g. mucus, HCO3, PG

What may contribute imbalance ?:

What may contribute imbalance ? Helicobacter pylori NSAIDs Ethanol Tobacco Severe physiologic stress (Burns, CNS trauma, Surgery, Severe medical illness) Steroids

Negative Feedback Regulation of Acid Secretion :

Negative Feedback Regulation of Acid Secretion Antral distention Protein content intragastric PH Gastrin release somatostatin secretion Increased gastric acid secretion Intragastric PH CGPR release CGPR= calcitonin gene related peptide

Pathophysiology:

Pathophysiology A peptic ulcer is a mucosal break, 3 mm or greater in size with depth, that can involve mainly the stomach or duodenum.

Pathophysiology:

Pathophysiology Two major variants in peptic ulcers are commonly encountered in the clinical practice: Duodenal Ulcer (DU) Gastric Ulcer (GU)

Phases of gastric secretion:

Phases of gastric secretion Phase Stimuli Pathway Cephalic (stimulate) Sight, smell, taste or thought of food Vagus (M3 receptors) Histamine (H2 receptor) Gastrin Gastric (stimulate) Food in the stomach Stretch: local reflex (M3 receptors) Chemical substances in food (gastrin) Increase pH: Inhibition of somatostatin (GHIH) release Intestinal (inhibit) Chyme in the duodenum

What is Peptic Ulcer ?:

What is Peptic Ulcer ? A peptic ulcer disease or PUD is an ulcer (defined as mucosal erosions equal to or greater than 0.5 cm) of an area of the gastrointestinal tract exposed to the acid and pepsin secretion Gastritis is the precursor to PUD and it is clinically difficult to differentiate the two Stomach (called gastric ulcer) Duodenum (called duodenal ulcer) Esophagus (called Esophageal ulcer) Meckel's Diverticulum (called Meckel's Diverticulum ulcer)

Recurrence :

Recurrence Risk factors for recurrence include: Non-ulcer dyspepsia Persistence of chronic gastritis after eradication therapy Female gender Intellectual disability Younger age High rates of primary infection Higher urea breath test values ABLES A Z et al. American Family Physician. 2007

Duodenal Vs Gastric Ulcers :

Duodenal Vs Gastric Ulcers Duodenal Age: 25-75 years Gnawing or burning upper abdomen pain relieved by food but reappears 1-3 hrs after meals Worse pain when stomach empty Bleeding occurs with deep erosion Hematemesis Melena Gastric Age: 55-65 years Relieved by food but pain may persist even after eating Anorexia, wt loss, vomiting Infrequent or absent remissions Small % become cancerous Severe ulcers may erode through stomach wall

Why Ulceration Occurs? :

Why Ulceration Occurs? High [H+] in the gastric lumen Require defense mechanisms to protect oesophagus and stomach Oesophagus – LES Stomach: a number of mechanisms Mucus secretion: slows ion diffusion Prostaglandins: I 2 and E 2 (alcohol, aspirin, and other drugs) Bicabonate ions High Blood Flow (nitric oxide)

H. pylori:

H. pylori Gram (-) rod with flagella H pylori is most common cause of PUD Transmission route fecal-oral Secretes urease → convert urea to ammonia Produces alkaline environment enabling survival in stomach Almost all duodenal and 2/3 gastric ulcer pt’s infected with HP Considered class 1 carcinogen → gastric cancer Higher prevalence in Low SES

Who are they ?:

Who are they ? Barry J Marshall J. Robin Warren Nobel Laureates of Medicine – 2005 Discovery of H. pylori & its role in peptic ulcer

Differentiating between H. pylori and NSAID-induced ulcer :

Differentiating between H. pylori and NSAID-induced ulcer Ulcers associated with H. pylori More often in duodenum Often superficial Less severe GI bleeding Ulcers associated with NSAIDs More often in stomach Often deep More severe GI bleeding Sometimes asymptomatic

PowerPoint Presentation:

Drugs of Ulcer treatment

PowerPoint Presentation:

Proglumide ACh PGE 2 Histamine Gastrin Adenyl cyclase _ + ATP cAMP Protein Kinase (Activated) Ca ++ + Ca ++ Proton pump K K + H + Gastric acid Parietal cell Lumen of stomach Antacid Omeprazole Ranitidine H 2 M 3 Misoprostol _ _ _ _ + PGE receptor + + Gastrin receptor + + +

Peptic Ulcers:

Therapy Purpose Therapy is directed at enhancing host defense or eliminating aggressive factors; i.e., H. pylori Peptic Ulcers

Classification:

Classification Acid Neutralizing agents: (ANTACIDS) Systemic: Sodium Bicarbonate and Sod. Citrate Nonsystemic: Magnesium hydroxide, Mag. Treisilicate, Aluminium hydroxide gel, Magaldrate and calcium carbonate Reduction in Gastric acid secretion: H2 antihistamines: Cimetidine, Ranitidine, Famotidine, Nizatidine and Roxatidine Proton pump inhibitors: Omeprazole, Lansoprazole Pantoprazole, Rabeprazole and Esomeprazole Anticholinergics: Pirenzepine, Propantheline and Oxyphenonium Prostaglandin analogue: Misoprostol

Classification – contd.:

Classification – contd. Ulcer protectives: Sucralfate, Colloidal Bismuth sudcitrate Anti-H. pylori Drugs: Amoxicillin, Clarithromycin, metronidazole, tinidazole and tetracycline

Antacids:

Antacids Weak bases that neutralize acid Also inhibit formation of pepsin (As pepsinogen converted to pepsin at acidic pH) Acid Neutralizing Capacity: Potency of Antacids Expressed in terms of Number of mEq of 1N HCl that are brought down to pH 3.5 in 15 minutes by unit dose of a preparation (1 gm)

Antacids - The Oldest Remedy:

Antacids - The Oldest Remedy Sodium Bicarbonate: Potent neutralizing capacity and acts instantly ANC: 1 gm = 12 mEq NOT USED ANYMORE FOR ITS DEMERITS: Systemic alkalosis Distension, discomfort and belching – CO 2 Rebound acidity Sodium overload

Antacids:

Antacids Present day antacids : Aluminium Hydroxide (ANC 1-2.5mEq/g) Magnesium Hydroxide (ANC 30 mEq) – milk of magnesia Magnesium trisilicate (ANC 1mEq/g) Duration of action : 30 min when taken in empty stomach and 2 hrs when taken after a meal Side effects : Aluminium antacids – constipation (As they relax gastric smooth muscle & delay gastric emptying) – also hypophosphatemia and osteomalcia Mg2+ antacids – Osmotic diarrhoea In renal failure Al3+ antacid – Aluminium toxicity & Encephalopathy (Magaldrate – hydrated hydroxy magnesium aluminate)

Antacids – contd.:

Antacids – contd. Simethicone : Decrease surface tension thereby reduce bubble formation - added to prevent reflux Alginates: Form a layer of foam on top of gastric contents & reduce reflux Oxethazaine: Surface anaesthetic

Therapeutic Questions:

Therapeutic Questions Is it rational to combine Aluminium hydroxide and magnesium hydroxide in antacid preparations ? How to avoid formation of insoluble complexes of drugs by antacids, that are not absorbed ?

Answers (!):

Answers (!) Interactions can be avoided by taking antacids 2 hrs before or after ingestion of other drugs Combination provides a relatively fast and sustained neutralizing capacity (Magnesium Hydroxide – Rapidly acting Aluminium Hydroxide - Slowly acting ) Combination preserves normal bowel function (Aluminium Hydroxide – constipation Magnesium hydroxide – diarrhoea )

The Reality:

The Reality Not part of Physician prescribed regimen – frequency of dosing and rebound acidity Over the counter (OTC) drug for symptomatic relief of dyspepsia May only be prescribed for very short term: Non-ulcer dyspepsia and minor episodes of heart burn As adjuvant in GERD – quick relieve

Sucralfate – ulcer protective:

Sucralfate – ulcer protective Salt of sucrose complexed to sulfated aluminium hydroxide (basic aluminium salt) MOA: In acidic pH polymerises to viscous gel that adheres to ulcer crater - more on duodenal ulcer Precipitates protein on surface proteins and acts as physical barrier Dietary proteins get deposited on this layer forming another coat Delays gastric emptying and causes gastric PG synthesis – protective action

Sucralfate – contd.:

Sucralfate – contd. Taken on empty stomach 1 hr. before meals Concurrent antacids, H 2 antagonist avoided (as it needs acid for activation) Uses: NSAID induced ulcers Patients with continued smoking ICU Topically – burn, bedsore ulcers, excoriated skins Dose: 1 gm 1 Hr before meals ADRs: Constipation, hypophosphatemia

Chemical reactions of antacids with HCl in the stomach:

Chemical reactions of antacids with HCl in the stomach

Antacids:

Antacids Capsules & Tablets: Powders Chewable tablets Suspensions Effervescent granules and tablets

H2 Antagonists:

H 2 Antagonists Cimetidine, Ranitidine, Famotidine, Roxatidine, Nizatidine and MOA: Reversible competitive inhibitors of H 2 receptor Highly selective, no action on H 1 or H 3 receptors All phases of gastric acid secretion Very effective in inhibiting nocturnal acid secretion (as it depends largely on Histamine ) Modest impact on meal stimulated acid secretion (as it depends on gastrin, acetylcholine and histamine) Volume of pepsin content and IF are also reduced Volume reduced by 60 – 70% - anti ulcerogenic effect No effect on motility

H2 antagonists:

H 2 antagonists Kinetics: All drugs are absorbed orally adequately Bioavailability upto 80 % Absorption is not interfered by presence of food Can cross placental barrier and reaches milk Poor CNS penetration 2/3 rd of the drugs are excreted unchanged in bile and urine Preparations: available as tablets, injections

H2 antagonists - ADRs:

H 2 antagonists - ADRs Extremely safe drugs and well tolerated Main ADRs are related to Cimetidine: Antiandrogenic effects Increases prolactin secretion and inhibits degradation of estradiol by liver Cytochrome P450 inhibition – theophylline, metronidazole, phenytoin, imipramine etc. Antacids Others: Headache, dizziness, bowel upset, dry mouth Bolus IV – release histamine – bradycardia, arrhythmia, cardiac arrest Elderly - precaution

H2 antagonists - Uses:

H 2 antagonists - Uses Promote the healing of gastric and duodenal ulcers Duodenal ulcer – 70 to 90% Gastric Ulcer – 50 to 75% (NSAID ulcers)) Stress ulcer and gastritis GERD Zollinger-Ellison syndrome Prophylaxis of aspiration pneumonia Urticaria Doses: 300 mg/40 mg/150 mg at bed time of R, F, Rox respectively for healing Maintenance: 150/20/150 mg BD of R, F, Rox

H2 blockers Tablets in Peptic ulcer :

H 2 blockers Tablets in Peptic ulcer Cimetidine 800mg bedtime /400mgBd 400mg bedtime Ranitidine 300 mg bedtime/150mg BD 150 mg bedtime Famotidine 40 mg bedtime 20 mg bedtime Roxatidine 150 mg bedtime 75 mg bedtime

Question:

Question Your friend wants to take a H 2 antagonist before he takes alcohol to avoid gastric irritation .He consults you .Which H 2 antagonist will you ask him to take ? Ranitidine/Famotidine/Roxatidine/Tiznidine ?

H2 antagonists – contd.:

H 2 antagonists – contd. Answer : Famotidine Explanation : All H 2 antagonist except famotidine inhibit gastric first pass metabolism of ethanol and increase its bioavailability

Proton Pump Inhibitors:

Proton Pump Inhibitors Most effective drugs in antiulcer therapy Prodrugs requiring activation in acid environment Block enzymes responsible for secreting HCl - binds irreversibly to H+K+ATPase Prototype: Omeprazole (Prilosec) Examples: Lansoprazole Pantoprazole Rabeprazole Esomeprazole Omeprazole

Question:

Question Half life of proton pump inhibitors is 1.5 hours only and these drugs are generally given once daily. How this can be justified ? Answer : P.P.I - Irreversible inhibitors of H+K+ATPase (Hit and run drugs)

Pharmacokinetics - PPI:

Pharmacokinetics - PPI Given on an empty stomach because food affects absorption They should be given 30 minutes to 1 hour before food intake because an acidic pH in the parietal cell acid canaliculi is required for drug activation, and food stimulates acid production Concomitant use of other antisecretory drugs - H2 receptor antagonists – reduces action Highly protein bound and rapidly Metabolized by the liver by CYP2C19 and CYP3A4 – dose reduction necessary in severe hepatic failure Excreted in Kidneys minimally (no dose reduction needed in renal failure and elderly)

Adverse Effects:

Adverse Effects The most common are GIT troubles in the form of nausea, abdominal pain, constipation, flatulence, and diarrhea Subacute myopathy, arthralgias, headaches, and skin rashes Prolonged use: Gynaecomastia, erectile dysfunction Leucopenia and hepatic dysfunction Vitamin B12 deficiency Hypergastrinemia which may predispose to rebound hypersecretion of gastric acid upon discontinuation of therapy and may promote the growth of gastrointestinal tumors (carcinoid tumors )

PowerPoint Presentation:

Therapeutic uses: Gastroesophageal reflux disease (GERD) Peptic Ulcer - Gastric and duodenal ulcers Bleeding peptic Ulcer Zollinger ellison Syndrome Prevention of recurrence of nonsteroidal antiinflammatory drug (NSAID) - associated gastric ulcers in patients who continue NSAID use. Reducing the risk of duodenal ulcer recurrence associated with H. pylori infections Aspiration Pneumonia

PPI – Dosage schedule:

PPI – Dosage schedule Omeprazole 20 mg o.d. Lansoprazole 30 mg o.d. Pantoprazole 40 mg o.d. Rabeprazole 20 mg o.d. Esomeprazole 20 - 40 mg o.d.

Muscarinic antagonists:

Muscarinic antagonists Atropine: Block the M 1 class receptors Reduce acid production Abolish gastrointestinal spasm Pirenzepine and Telenzepine Mechanism of action: Reduce meal stimulated HCl secretion by reversible blockade of muscarinic (M1) receptors on the cell bodies of the intramural cholinergic ganglia (receptors on parietal cells are M3). Unpopular as a first choice because of high incidence of anticholinergic side effects (dry mouth and blurred vision)

Prostaglandin analogues:

Prostaglandin analogues Inhibit gastric acid secretion Exhibit ‘cytoprotective’ activity Enhance local production of mucus or bicarbonate Promote local cell regeneration Help to maintain mucosal blood

Prostaglandin analogues - Misoprostol:

Prostaglandin analogues - Misoprostol Actions: Inhibit histamine-stimulated gastric acid secretion Stimulation of mucin and bicarbonate secretion Increase mucosal blood flow (Reinforcing of mucous layer buffered by HCO3 secretion from epithelial cells) Therapeutic uses: Prevent ion of NSAID-induced mucosal injury (rarely used because it needs frequent administration – 4 times daily)

Misoprostol:

Misoprostol Doses: 200 mcg 4 times a day (Misoprost) ADRs: Diarrhoea and abdominal cramps Uterine bleeding Abortion Exacerbations of inflammatory bowel disease and should be avoided in patients with this disorder Contraindications: Inflammatory bowel disease Pregnancy (may cause abortion)

Question:

Question A patient comes to your clinic at midnight complaining of heart burn. You want to relieve his pain immediately. What drug will you choose?

Answer is:

Answer is Antacids Explanation : Antacids neutralize the already secreted acid in the stomach. All other drugs act by stopping acid secretion and so may not relieve symptoms atleast for 45 min

PowerPoint Presentation:

Eradication of H.pylori Omeprazole Amoxicillin Clarithromycin Metronidazole

PowerPoint Presentation:

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 – 10 days not very effective

PowerPoint Presentation:

Triple Therapy – cont … Bismuth subsalicylate – 2 tab qid Metronidazole - 250 mg qid Tetracycline - 500 mg qid Some other Triple Therapy Regimens are Ranitidine Bismuth citrate - 400 mg bd Tetracycline - 500 mg bd Clarithromycin / Metronidazole - 500 mg bd

Bismuth subsalicylate:

Bismuth subsalicylate Pharmacological actions: Undergoes rapid dissolution in the stomach into bismuth and salicylates Salicylates are absorbed Bismuth coats ulcers and erosions protecting them from acid and pepsin and increases prostaglandin and bicarbonate production Uses: Treatment of dyspepsia and acute diarrhoea

PowerPoint Presentation:

Question A pregnant lady (first trimester) comes to you with peptic ulcer disease. Which drug will you prescribe for her ?

PowerPoint Presentation:

Answer : Antacids or Sucralfate Explanation ; H 2 antagonists cross placenta and are also secreted in breast milk. Safety of Proton pump inhibitors not established in pregnancy. Misoprostol causes abortion

PowerPoint Presentation:

Stress induced ulceration after head trauma -Cushing’s ulcer Stress induced ulceration after severe burns - Curling’s ulcer

Etiology:

Etiology Other uncommon causes include: Gastrinoma (Gastrin secreting tumor) Stress ulceration (trauma, burns, critical illness) Viral infections Vascular insufficiency

Etiology :

Etiology The two most common causes of PUD are: Helicobacter pylori infection ( 70-80%) Non-steroidal anti-inflammatory drugs (NSAIDS)

PowerPoint Presentation:

1. Etiology – Helicobacter pylori

H.pylori Epidemiology:

H.pylori Epidemiology One half of world’s population has H.pylori infection, with an estimated prevalence of 80-90 % in the developing world The annual incidence of new H. pylori infections in industrialized countries is 0.5% of the susceptible population compared with ≥ 3% in developing countries

H.pylori as a cause of PUD:

H.pylori as a cause of PUD The majority of PUD patients are H. pylori infected

H.pylori as a cause of PUD:

H.pylori as a cause of PUD 95% 85%

Pathogenesis of H. pylori infection :

Pathogenesis of H. pylori infection H. pylori is Gram-negative, spiral & has multiple flagella at one end Transmitted from person-to-person by Oro–oral or feco -oral spread No reservoir in animal or water supply

Pathogenesis of H. pylori infection:

Pathogenesis of H. pylori infection The Flagellae make it motile, allowing it to live deep beneath the mucus layer It uses an adhesin molecule to bind to epithelial cells Where the pH there is close to neutral

Pathogenesis of H. pylori infection:

Pathogenesis of H. pylori infection Any acidity is buffered by the organism's production of the enzyme urease, which catalyzes the production of ammonia (NH3) from urea & raises the pH there The bacterium stimulates chronic gastritis by provoking a local inflammatory response.

Pathogenesis of H. pylori infection:

Pathogenesis of H. pylori infection In the cellular level: H. pylori express cagA & vacA genes cagA gene  signals to the epithelial cells involving: - Cell replication, - Apoptosis, & - Morphology

Pathogenesis of H. pylori infection:

Pathogenesis of H. pylori infection In the cellular level: vacA gene  producing a pore-forming protein, which has many destructing effect to the epithelium like: - ↑Cell permeability & efflux of micronutrients, - Induction of apoptosis, & - Suppression of local cell immunity

Pathogenesis of H. pylori infection:

Pathogenesis of H. pylori infection - ↓ Somatostatin production from antral D-cells due to antral gastritis Low somatostatin will ↑ Gastrin release from G-cell  hypergastrinemia This will stimulate acid production by the parietal cells  leading to further duodenal ulceration. Effects of H. pylori on gastric Hormones This effect is exaggerated among smokers!

Carcinogenic effect of H. pylori :

Carcinogenic effect of H. pylori H. pylori Host Factors Other environmental Factors Antral gastritis Pangastritis DU GU Gastritis Cancer

Carcinogenic effect of H. pylori:

Carcinogenic effect of H. pylori Epidemiologic evidence suggests that infection with HP is associated with >2 fold increase risk of gastric cancer However due to uncertainty regarding the benefit of HP eradication on reducing cancer risk, wide-spread screening for HP in asymptomatic individuals cannot be recommended at this time

PowerPoint Presentation:

For persons at high risk for gastric cancer (e.g., first degree relatives) screening can be considered on a case by case basis ABLES A Z et al. American Family Physician. 2007

PowerPoint Presentation:

2. Etiology -Non-Steroidal Anti-inflammatory Drugs (NSAIDS)

NSAIDS:

NSAIDS Symptomatic GI ulceration occurs in 2% - 4% of patients treated with NSAIDs for 1 year In view of the million of people who take NSAIDs annually, these small percentages translate into a large number of symptomatic ulcers The effects of aspirin & NSAIDs on the gastric mucosa ranges from mucosal hemorrhages to erosions & acute ulcers

NSAIDS:

NSAIDS Inhibits the production of prostaglandins precursor from membrane fatty acids resulting in: 1. Decrease mucus & HCO3 production 2. Decrease mucosal blood flow 3. Reduce cell renewal The drugs also generate oxygen-free radicals & products of the lipoxygenase pathway that may contribute to ulceration

NSAIDS:

NSAIDS Gastric acid probably aggravates NSAID-induce mucosal injury by - Converting superficial injury to deeper mucosal necrosis, - Interfering with haemostasis & platelet aggregation - Impairing ulcer healing

NSAIDS:

NSAIDS Users of NSAIDs are at approximately 3 times greater relative risk of serious adverse gastrointestinal events than nonusers

NSAIDS:

NSAIDS Identify risk factors: Age > 65 years (3.5-fold increased risk) Smoking Previous history of GI event (e.g. ulcer bleeding 4-fold increase risk) Concomitant drug use Anticoagulants ( eg, warfarin; 3-fold increase) Corticosteroid ( 2-fold increase) Low dose aspirin alone ( 2.5-fold increase) Aspirin + NSAIDS (4-fold increase vs aspirin alone)

Type of NSAID & Risk of Ulcer:

Type of NSAID & Risk of Ulcer Risk Group Drug Relative Risk Low Ibuprofen Diclofenac 2.0 4.2 Medium Naproxen Indomethacin Piroxicam 9.1 11.3 13.7 High Ketoprofen Azapropazone 23.7 31.5

Clinical Presentation:

Clinical Presentation Recurrent epigastric pain (the most common symptom) Burning Occurs 1-3 hours after meals Relieved by food  DU Precipitated by food  GU Relieved by antacids Radiate to back (consider penetration) Pain may be absent or less characteristic in one-third of patients especially in elderly patients on NSAIDs

Clinical Presentation:

Clinical Presentation Nausea, Vomiting Dyspepsia, fatty food intolerance Chest discomfort Anorexia, weight loss especially in GU Hematemesis or melena resulting from gastrointestinal bleeding

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Diagnosis of PUD

Peptic Ulcer Disease:

Peptic Ulcer Disease Diagnosis: Diagnosis of ulcer Diagnosis of H. pylori

Diagnosis of PUD:

Diagnosis of PUD In most patients routine laboratory tests are usually unhelpful Diagnosis of PUD depends mainly on endoscopic and radiographic confirmation

Doudenal Ulcer on Endoscopy:

Doudenal Ulcer on Endoscopy Doudenal Ulcer Normal doudenal bulb

Gastric Ulcer on Endoscopy:

Gastric Ulcer on Endoscopy Chronic Gastric Ulcers

Diagnosis of H. pylori:

Diagnosis of H. pylori Non-invasive C 13 or C 14 Urea Breath Test Stool antigen test H. pylori IgG titer (serology) Invasive Gastric mucosal biopsy Rapid Urease test

Diagnosis of H. pylori:

Diagnosis of H. pylori Non-invasive 1. C13 or C14 Urea Breath Test The best test for the detection of an active infection

Diagnosis of H. pylori:

Diagnosis of H. pylori Non-invasive Serology for H pylori Serum Antibodies (IgG) to H pylori (Not for active infection) Fecal antigen testing ( Test for active HP )

Diagnosis of H. pylori:

Diagnosis of H. pylori Invasive Upper GI endoscopy Highly sensitive test Patient needs sedation Has both diagnostic & therapeutic role

Diagnosis of H. pylori:

Diagnosis of H. pylori Invasive ( endoscopy) Diagnostic : Detect the site and the size of the ulcer, even small and superficial ulcer can be detected Detect source of bleeding Biopsies can be taken for rapid urease test , histopathology & culture

Diagnosis of H. pylori:

Diagnosis of H. pylori Invasive ( endoscopy) Rapid urease test ( RUT) Considered the endoscopic diagnostic test of choice Gastric biopsy specimens are placed in the rapid urease test kit. If H pylori are present, bacterial urease converts urea to ammonia, which changes pH and produces a C O L O R change

Diagnosis of H. pylori:

Diagnosis of H. pylori Invasive ( endoscopy) * Histopathology Done if the rapid urease test result is negative * Culture Used in research studies and is not available routinely for clinical use

TREATMENT OF PUD:

TREATMENT OF PUD DRUG TYPE EXAMPLES DOSE ACID-SUPPRESSING DRUGS ANTACIDS MYLANTA, MAALOX, TUMS, GAVISCON 100-140 MEQ/L 1 H AND 3 H AFTER MEALS H2 RECEPTOR ANTAGONIST CIMETIDINE RANITIDINE FAMOTIDINE NIZATIDINE CIME-RANI-FAMO-NIZA 400 MG BID 300 MG HS 40 MG HS 300 MG HS PROTON PUMP INHIBITORS- MOST POTENT ACID INHIBITORY AGENTS AVAILABLE OMEPRAZOLE LANSOPRAZOLE RABEPRAZOLE PANTOPRAZOLE ESOMEPRAZOLE REPOL 20 MG/D 30 MG/D 20 MG/D 40 MG/D 20 MG/D

TREATMENT OF PUD:

TREATMENT OF PUD Drug Type Examples Dose MUCOSAL PROTECTIVE AGENTS SUCRALFATE – ACTS AS A PHYSICOCHEMICAL BARRIER, PROMOTE TROPHIC ACTION BY BINDING GROWTH FACTORS SUCH AS EGF, ENHANCING PROSTAGLANDIN SYNTHESIS, STIMULATING MUCOUS AND BICARBONATE SECRETION, AND ENHANCING MUCOSAL DEFENSE AND REPAIR SUCRALFATE 1 g qid

TREATMENT OF PUD:

TREATMENT OF PUD PROSTAGLANDIN ANALOGUE – ENHANCEMENT OF MUCOSAL DEFENSE AND REPAIR MISOPROSTOL 200ΜG QID BISMUTH-CONTAINING COMPOUNDS – ULCER COATING, BINDING OF PEPSIN, STIMULATION OF PROSTAGLANDINS, HCO3, AND MUCOUS SECRETION BISMUTH SUBSALICYLATE (BSS) – MOST IDELY USED PREPARATIONS DRUG TYPE EXAMPLES DOSE

THERAPY OF H. pylori:

THERAPY OF H . pylori REGIMENS RECOMMENDED FOR ERADICATION OF H. PYLORI INFECTION DRUG DOSE (RESPECTIVELY) TRIPLE THERAPY BSS + METRONIDAZOLE + TETRACYCLINE RANITIDINE BISMUTH CITRATE + TETRACYCLINE + CLARITHROMYCIN OR METRONIDAZOLE OMEPRAZOLE (LANSOPRAZOLE) + CLARITHROMYCIN + METRONIDAZOLE OR AMOXICILLIN 2 TABLETS QID, 250 MG QID, 500 QID 400 MG BID, 500 MG BID, 500 MG BID 20 MG BID, 250/500 MG BID, 500 MG BID, OR 1 G BID QUADRUPLE THERAPY OMEPRAZOLE (LANSOPRAZOLE) BISMUTH SUBSALICYLATE METRONIDAZOLE TETRACYCLINE 20 MG (30 MG) DAILY 2 TABLETS QID 250 MG QID 500 MG QID

SURGICAL :

SURGICAL MANAGEMENT

DUODENAL ULCER:

DUODENAL ULCER

RATIONALE:

RATIONALE EXCLUDING THE THE DAMAGING EFFECTS OF ACID FROM THE DUODENUM BY DIVERSION OF ACID AWAY FROM DUODENUM REDUCING THE SECRETORY POTENTIAL OF STOMACH (OR) BOTH

BILLROTH 2 GASTRECTOMY:

BILLROTH 2 GASTRECTOMY BILLROTH 1 ST IN 1881 1 ST GJ IN SAME YEAR BY WOLFER BILLROTH 1 GASTRECTOMY+GASTRODUODENAL ANASTOMOSIS BILLROTH 2 GASTRECTOMY +DUODENUM CLOSED+RETROCOLIC GJ WITH AS SMALL AN AFFERENT LOOP GASTROJEJUNOSTOMY TRUNCAL VAGOTOMY & DRAINAGE SELECTIVE VAGOTOMY&DRAINAGE HIGHLY SELECTIVE VAGOTOMY

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SURGERY-RELATED COMPLICATIONS:

SURGERY-RELATED COMPLICATIONS Afferent Loop Syndromes – caused by an incomplete drainage of bile and pancreatic secretions from an afferent loop that is partially obstructed in patients who have undergone partial gastric resection with Billroth II anastomosis resulting in bacterial overgrowth secondary to stasis manifested by abdominal pain, bloating, and diarrhea with concomitant malabsorption of fats and vitamin B12

SURGERY-RELATED COMPLICATIONS:

SURGERY-RELATED COMPLICATIONS Dumping Syndrome – consists of a series of vasomotor and GI SSx and occurs in Pxs who have undergone vagotomy and drainage 2 phases early dumping (15-30 min after meals) SSx are crampy abdominal discomfort, nausea, diarrhea, belching, tachycardia, palpitations, diaphoresis, light-headedness, and rarely, syncope late dumping (90 min – 3 h after meals) SSx are light-headedness, diaphoresis, palpitations, tachycardia, and syncope, SSx is a result of rapid emptying of hyperosmolar gastric contents into the small intestine, resulting in a fluid shift into the gut lumen

SURGERY-RELATED COMPLICATIONS:

SURGERY-RELATED COMPLICATIONS Postvagotomy Diarrhea – mc observed after truncal vagotomy manifested as intermittent diarrhea that occurs typically 1-2 h after meals Bile Reflux Gastropathy – present with abdominal pain, early satiety, N/V, and mucosal erythema of the gastric remnant in a subset of post-partial gastrectomy patients Maldigestion and Malabsorption , Gastric Adenocarcinoma

Type I:

Type I Occur at the incisura. Not associated with hyperacidity, most patients have low acid output. Associated with ABO group “A”.

Type II:

Type II A combination of 2 ulcers, one in the body of the stomach, the other in the duodenum. Usually occur in hypersecretory states. Associated with ABO “O”.

Type III:

Type III Located pre-pyloric. Associated with hypersecretion. Type “O” blood association. Typically 2-3 cm from pylorus, can be multi.

Type IV:

Type IV Csendes type ulcers. Occur high on lesser curve at/near the GE junction. Not associated with hypersecretion. Usually result from defective mucosal defense.

Type V:

Type V Can occur anywhere in stomach. Result from chronic ASA/NSAID ingestion.

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H. pylori Thank U 

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