Peptic ulcer disease

Notes

## Basic introduction

  • Peptic ulcer disease (PUD) is an erosion that penetrates through the muscularis mucosae in the stomach (that results in gastric ulcer) or the first section of the duodenum (that results in duodenal ulcer) causing ulcers that tend to be chronic and recurrent.

## Outline of the pathogenesis of peptic ulcers

  • There is usually a delicate physiological balance [such as tight intercellular junctions, mucosal blood flow, mucus, cellular restitution, and epithelial regeneration] between peptic acid secretion and gastroduodenal mucosal defense. Peptic ulcer occurs when this balance is disrupted by the following factors:

_Helicobacter pylori infections in GIT

_Abnormality in secretion of gastric acid and pepsin

_Gastrinoma in Zollinger-Ellison syndrome.

_Mastocytosis [a rare disorder in which excessive number of mast cells are produced]

_Basophilic leukemias

_Cholinergic hypersensitivity and parasympathetic dominance.

_G-cell hyperplasia

_An increase in parietal-cell mass

_Physiological imbalance between  gastrin and somatostatin [which have antagonistic effects]

_Psychologic stress

_Cigarette smoking and /or alcohol consumptlion

_Drugs such as NSAIDs, oral bisphosphonates, immunosuppressants.

## H. pylori is by far the most important cause of peptic ulcers (causing at least 95% of duodenal ulcers). These bacteria cause these ulcers by:

  • Destroying the mucosal defense system [where it reduces the thickness of the mucus gel layer]
  • Increasing gastric acid secretion
  • Reducing mucosal blood flow
  • Interacting with the gastric epithelium.
  • Production of various antigens, virulence factors, and soluble mediators
  • Induction of inflammation that leads to secretion of more hydrochloric acid by increasing parietal-cell mass
  • Activation of pylori cytotoxin-associated gene, CagA, that regulates cellular responses could result in apical junction barrier disruption, IL-8 secretion as well as phenotypic changes to gastric epithelial cells.
Symptoms
  • A good number of patients, especially the elderly, are asymptomatic (and they may present the first time with complications)
  • Epigastric pain (mostly at night and when hungry for DU and after meals sometimes for GU)
  • Bloating, vomiting, nausea (especially due to obstruction that results from edema and scarring of ulcers, especially pyloric channel ulcers).

## Complications of Peptic Ulcer Disease

  • in Hemmorrhage: it occurs in 20-30% of PUDs. It is best detected by endoscopy.
  • Perforation: it occurs in about 10% patients with PUDs (but less in cases of gastric ulcers), in about 75% cases erect chest X-ray show free gas the peritoneum.
  • Subphrenic collection or abscess (which is the accumulation of infected fluid between the diaphragm, the liver and the spleen). It is best by CT scanning or less frequently by X-ray.
  • Gastric outlet obstruction: the cause of obstruction can be scaling, inflammation, and / or spasm, especially in pyloric channel ulcers).
  • Gastric cancer: pylori ulcers increase the risk of gastric cancers by a factor of 3-6.
  • Hematemesis
Diagnosis
  • Barium meal X-ray
  • Stool for occult blood
  • Stool for pylori antigen using rapid tests
  • Endoscopy (of upper GIT)
  • Biopsy (during endoscopy) of gastric mucosa for Pylori and eliminating the possibility of gastric or duodenal cancers.
  • Serum gastrin levels (sometimes).
  • CT scanning and chest X-ray for detection of complications of PUD.
  • Physical examination, especially for the signs of obstruction that include succussion splash head at about 6hrs after meal; food residual after overnight fasting (more than 200 mL).
Management
  • Antisecretory therapy
  • The more preferred triple therapy for pyloriinfection. Use of proton pump inhibitor [PPI]-based triple therapy tends to give the best results. PPI are combined with amoxicillin [or less preferred metronidazole or tinidazole due to higher resistance rates] and clarithromycin and the treatment is carried out for 7-14 days or more in complicated cases.
  • Surgical interventions

## Drugs that are used to treat dyspepsia, reflux and peptic ulcers are classified into the following categories:

  • Antacids and antiflatulants e.g. aluminum, calcium and magnesium salts.
  • Drugs that protect ulcers and promote healing g. sucralfate, colloidal bismuth and carbenoxolone
  • Drugs that lower secretion of HCl e.g. H2-antagonists [such as cimetidine, ranitidine, famotidine and nizatidine], proton pump inhibitors[such as omeprazole, esomeprazole, and lansoprazole], anticholinergics [such as pirenzipine]and prostaglandins analogues such as misoprostal]
  • Drugs that act on pylori e.g. triple therapy of proton pump inhibitors and amoxicillin, clarithromycin or metronidazole.

## Therapeutics guided by Essential Drug List consideration

  • Magnesium trisilate compound tablets
  • Omeprazole tablets 20mg
  • Ranitidine tablets 150mg
  • Ranitidine injection 50mg/2mL

## Standard doses of drus  in the Essential Drug List

  • Magnesium trisilate compound tablets: person over 14 years: chew 1 or 2 tablets TID, one hour after meals and at bedtime or as required. Children 10-14 years: chew 1 TID.
  • Omeprazole: Dose: Benign gastric ulcer; 20mg OD x 8/52. Benign duodenal ulcer; 20mg OD x 4/52. In severe cases doses are doubled. Reflux oesophagitis; 20mg OD x 4/52 or more. Zollinger Ellison Syndrome; 20-120mg daily [above 80mg]. It is given in two divided doses.
  • Ranitidine: Peptic ulcer: 300mg nocte 4/52. Maintenance: 150mg nocte. Children over 18 years: 150mg BD. Not recommended for children below 8yrs. Zollinger-Ellison syndrome: 150mg TID up to 6g daily if necessary, in divided doses. Inj. Adults: 50mg by slow 1.V inj or inf. or I.M [repeat six or eight hourly].

## Therapeutics using drugs that are NOT in the Essential Drug List

  • Cytoprotective agents

_Sucralfate: 12 years and above: 2g BD [on rising and at bedtime] or 1g QID 1 hour before meals and at bedtime, taken for 4-6 weeks or in resistant cases up to 12 weeks; max. 8g daily. Child 1 month - 2 years 250mg 4-6 times daily, 2-12 years 500mg 4-6 times daily, 12-18 years 1g 4-6 times daily.

  • H2-Antagonists

_Cimetidine: Benign gastric and duodenal ulcer: 400mg BD or 800mg at bedtime: long-term treatment: 400mg Nocte. Reflux oesophagitis: 800-1200mg divided into 2-4 daily doses. Zollinger Ellison Syndrome: 400mg QID or more. For hyperacidity, dyspepsia and heartburn: 100mg stat, repeat 100mg if symptoms persist for more than one hour.

_Famotidine: Benign gastric and duodenal ulcers treatment: 40mg Nocte 4-8 weeks. Maintenance: 20mg at night. Reflux oesophagitis, 20-40mg BD [6-12 weeks]. Zollinger-Ellison syndrome 20mg every 6 hours.

­_Ranitidine: Peptic ulcer: 300mg nocte 4/52. Maintenance: 150mg nocte. Children over 18 years: 150mg BD. Not recommended for children below 8yrs. Zollinger-Ellison syndrome: 150mg TID up to 6g daily if necessary, in divided doses. Inj. Adults: 50mg by slow 1.V inj or inf. or I.M [repeat six or eight hourly].

  • Proton Pump Inhibitors [PPIs]

_Esomeprazole: GERD without erosive esophagitis: 20 mg PO OD x 4 weeks, 20-40 mg OD IV up to 10 days, switch to PO once patient able to swallow. GERD with erosive esophagitis: Treatment: 20mg or 40 mg PO OD x 4-8 weeks. Maint: 20 mg PO OD up to 6 months, 20-40 mg OD IV up to 10 days, switch to PO once patient able to swallow. H. pylori eradication: Indicated for combination therapy [with amoxicillin and clarithromycin] to eradicate H. pylori in patients with duodenal ulcer 40 mg PO OD x 10 days, WITH amoxicillin 1000 mg PO BID, AND clarithromycin 500 mg PO BID x 10 days. Risk reduction of NSAID-associated gastric ulcer, 20-40 mg PO OD x up to 6 months. Zollinger-Ellison Syndrome, 60 mg PO OD [initial] up to 100 mg PO OD, OR 60 mg PO BID.

_Lansoprazole: Benign gastric ulcer: 30 mg daily in the morning for 8 weeks. Duodenal ulcer, 30 mg daily in the morning for 4 weeks; maintenance 15 mg daily. NSAID-associated duodenal or gastric ulcer: 30 mg OD for 4 weeks, continued for further 4 weeks if not fully healed; prophylaxis, 15–30 mg OD. Zollinger-Ellison syndrome [and other hypersecretory conditions]: initially 60 mg OD adjusted according to response; daily doses of 120 mg or more given in two divided doses. GERD: 30mg in the morning for 4 weeks, continued for further 4 weeks if not fully healed; maintenance 15-30mg daily. Acid-related dyspepsia: 15-30mg daily in the morning for 2-4 weeks. Child: body-weight under 30kg, 0.5-1 mg/kg [max. 15mg] once daily in the morning, body-weight over 30kg, 15-30mg OD in the morning.

_Omeprazole: Dose: Benign gastric ulcer; 20mg OD x 8/52. Benign duodenal ulcer; 20mg OD x 4/52. In severe cases doses are doubled. Reflux oesophagitis; 20mg OD x 4/52 or more. Zollinger Ellison Syndrome; 20-120mg daily [above 80mg]. It is given in two divided doses.

_Omeprazole / Sodium bicarbonate: Active duodenal ulcer for short term in adults: 20mg OD x 4 -8 wks. Benign gastric ulcer: 40mg OD x 4-8 wks. GERD: 20 mg OD for up to 4 wks. Erosive esophagitis: 20 mg OD for 4 - 8 wks.

_Pantoprazole: GERD: 40mg daily [up to 80 mg daily] for 4-8 wks. Gastric ulcer: 40mg daily [up to 80mg daily] for 4-8 wks.  Duodenal ulcer: 40mg daily [up to 80 mg daily] for up to 4 weeks.

_Rabeprazole:Benign gastric ulcer: 20mg OD x 6/52. Benign duodenal ulcer: 20mg OD x 4/52. GERD: 20mg OD x 4/52 or more.

  • Prostaglandin analogues

_Misoprostol: 200-800mcg QID.

  • Pylori elimination regimes

_Esomeprazole/Clarithromycin/Amoxicillin: One set of daily dose daily for 7 days

_Lansoprazole/Clarithromycin/Amoxicillin: One set of daily dose daily for 7 days

_Lansoprazole caps: 30mg BD x 1/52. Amoxicillin caps: 1000mg BD x 1/52. Clarithromycin tabs: 500mg BD x 1/52.

_Lansoprazole/Clarithromycin/Tinidazole One set of daily dose daily for 7 days.

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