Peptic ulcer, Classification of Antiulcer Drugs, Mechanism of action, Pharmacokinetics, Side effects, Drug interactions and Uses, MCQs for GPAT, NEET PG,NIPER, Drug inspector exam and pharmacist exam.

Peptic ulcer, Classification of Antiulcer Drugs, Mechanism of action, Pharmacokinetics, Side effects, Drug interactions and Uses, MCQs for GPAT, NEET PG,NIPER, Drug inspector exam and pharmacist exam.

PEPTIC ULER: Peptic ulcer are open sores that develop on the inner lining of the stomach and the upper portion of small intestine. It occurs in that part of the g.i.t which is exposed to gastric acid secretions.

Types of peptic ulcer: There are two types of peptic ulcer.

  1. Gastric ulcer: Open sores that develop on the inside lining of stomach.
  2. Duodenal ulcer: Open sores that develop on the inside lining of the upper portion of small intestine

Risk factors of peptic ulcer: 

  1. Helicobacter pylori bacteria (H. pylori): H. pylori is the most common cause of gastric and duodenal ulcers. This bacterium damages the mucus that protects your stomach and small intestine allowing for stomach acid to burn.
  2. Zollinger-Ellison Syndrome: It is a rare condition that affects the digestive tract. It is characterized by the formation of tumors, called gastrinomas. It produce excessive amounts of hormones called gastrin. Gastrin triggers overproduction of gastric Acid.
  3. Stress

Sign and symptoms: 

  1. Epigastric pain
  2. The pain tends to be worse at night and occurs 1 to 3hrs of the meal.
  3. Nausea, vomiting, significant weight loss.
  4. Belching(burping)
  5. Complications of hemorrhage in one third patients.
  6. Feeling of fullness.
  7. Pain or discomfort in upper abdomen
  8. Bloody or dark terry stools.

Classification of drugs:

A. Gastric acid secretion inhibitors:

  1. H2 Antihistamines: 

a. Cimetidine

b. Ranitidine

c. Famotidine

d. Roxatidine

e. Lafutidine

2. Anticholinergics:

a. Pirenzepine

b. Propantheline

c. Oxyphenonium

3. Proton pump inhibitors:

a. Omeprazole (Prototype)

b. Pantoprazole

c. Esomeprazole

d. Lansoprazole

e. Rabeprazole

f. Dexrabeprazole

g. Ilaprazole

4. Prostaglandin analogue:

a. Misoprostol

B. Gastric acid neutralizers (Antacid):

1. Systemic:

a. Sodium bicarbonate

b. Sodium citrate

2. Non systemic:

a. Mag. hydroxide

b. Mag. trisilicate

c. Alumin. hydroxide

d. Magaldrate

e. Calcium carbonate

C. Ulcer protectives:

a. Sucralfate

b. Colloidal bismuth subcitrate (CBS)

D. Anti H,pylori drugs:

a. Amoxicillin

b. Clarithromycin

c. Metronidazole

d. Tinidazole

e. Tetracycline

f. CBS

A. Gastric acid secretions inhibitors:

1.H2- Antihistamines:

a. Cimetidine:

First H2 blocker to be introduced clinically, described as ‘protoype’ drug. All clinically used H2 blockers are competitive antagonist of histamine except famotidine. These drugs block histamine- induced gastric acid secretions. Inhibit acid production by reversible competing with histamine for binding with H2 receptor on the basolateral membrane of parietal cells. Suppress acid production by 70%. Inhibit basal acid secretions and nocturnal secretion also.

Pharmacokinetis: Absorbed orally, bioavailability is 60-80% due to first pass hepatic metabolism. It crosses placenta and reaches milk, but poorer blood brain barrier. About 2/3rd drug is excreted unchanged in urine and bile. The t1/2 is of 2-3hr, but duration of action is longer.

Side effects: 1. Diarrohea, headache, drowsiness, fatigue, constipation.

2.Confusion, delirium, hallucinations, and slurred speech.

3. Rebound hyperacidity.

4. Thrombocytopenia.

5. Pancytopenia, neutropenia, anaemia.

Uses: Peptic ulcer, non ulcer dyspepsia, urticaria, GERD(gastroesophageal reflux disease), bleeding from stress ulcers and erosive gastritis.

 Drug interactions: Inhibit the metabolism of many drugs:

  1.  Theophylline
  2. Phenytoin
  3. Warfarin
  4. Carbamazepine
  5. Metronidazole

b. Ranitidine: Non-imidazole H2 blocker. 5 times more potent than cimetidine. Longer duration of action, with greater 24hr acid suppression is obtained. Less penetration in brain, less inhibition of hepatic metabolism of other drugs.

Side effects: Headache, diarrhea, constipation.

Uses: Used in peptic ulcer, GERD and urticaria.

c. Famotidine: Thiazole ring containing H2 blockers which bind tightly with H2 receptors and exhibit longer duration of action. Some inverse agonistic action has been demonstrated. 5-8 times more potent than cimetidine. Oral bioavailability is 40-50 %. it is excreted trough kidney 70% in unchanged form.

Side effects: Dizziness, bowel upset, headache, rashes

Uses: Peptic  ulcer, GERD.

d. Roxatidine: Same mechanism of action, pharmacokinetics  and side effects to that of rantidine. It is twice more potent and longer acting.

e. Lafutidine: This is second generation H2 blocker. It acts by preventing gastric acid secretions. It also activates calcitonin gene related peptide, resulting in the stimulation of nitric oxide (NO) and regulation of gastric mucosal blood flow, increases somatostatin levels also resulting in less gastric acid secretion.

Side effects: Constipation, diarrhea, drug rash, nausea, vomiting and dizziness.

Uses: Exact uses are not known but it can be use for gastric ulcers and duodenal ulcers, gastritis and chronic gastritis.

2. Proton pump inhibitors (PPIs): This the most commonly used class of acid suppressants.

a. Omeprazole: It is prototype member of benzimidazoles which inhibit the final step of gastric acid secretions. It is a powerful inhibitor of gastric acid. It has dose dependent suppression of gastric acid secretion without blocking any receptor. After absorption of prodrug it gets activate tetracyclic sulfonamide cation. This activated form then binds to sulfhydryl groups of cysteine in the H+ k+ ATPase, irreversibly inactivating the pump molecule. Especially when two molecule of omeprazole reacts with one molecule of the enzyme. It also inhibit gastric mucosal carbonic anhydrase.

Pharmacokinetics: All PPIs are enteric coated to protect the drug from molecular transformation in the acidic gastric juice. it as administered orally. Oral bioavailability is about 50% due to acid lability. Bioavailability of all PPI are reduced by food. So they should be taken in empty stomach, because 10% of proton pumps are active. Omeprazole is highly plasma protein bound drug. Rapidly metabolized in liver by CYP2C19 and CYP3A4. Plasma t1/2 is of 1hr. Metabolites are excreted in urine.

Side effects: These are very safer drugs. Some side effects are nausea, loose stools, headache, and dizziness.

Interactions: Inhibits oxidation of certain drugs:

  1. Diazepam
  2. Phenytoin
  3. Warfarin

Reduced gastric acidity decreases absorption of:

  1. ketoconazole
  2. Iron salts

Clarithromycin inhibits omeprazole metabolism.


  1. Peptic ulcer
  2. Bleeding peptic ulcer
  3. GERD
  4. Zollinger-Ellison Syndrome
  5. Stress ulcers
  6. Aspiration pneumonia

b. Pantoprazole: It has same potency like omeprazole. It is more stable and has higher oral bioavailability. Affinity for CYP450 is lower than omeprazole. It is use as i.v for bleeding peptic ulcer, and for prophylaxis of acute stress ulcers. also used foe peptic ulcer, stress ulcer, Zollinger- Ellison syndrome.

c. Esomeprazole: It is S-enantiomer of Omeprazole. Have higher bioavailability and better control of intra-gastric pH than omeprazole in GERD patients because of slower elimination and longer t1/2. It is provide healing effects in erosive gastritis and symptomatic relief in GERD. Side effects and drug interactions are similar to of omeprazole.

d. Lansoprazole: It has similar action like omeprazole. More potent then omeprazole. Reversible inhibition of H+K+ ATPase. It has higher oral bioavailability. Fastest onset of action and slightly longer t1/2 than omeprazole. Dose should be reduced in case of liver disease. Side effects are similar but less drug interactions, diazepam and phenytoin metabolism may be reduced.

e. Rabeprazole: It is the fastest acid suppressant drug. Due toe it’s higher pKa, it is more rapidly converted into active species. Potency and efficacy are exactly similar to omeprazole. No drug interaction have been observed.

f. Dexrabeprazole: It is active dextro-isomer of rabeprazole, produces similar acid suppression at half the dose.

g. Ilaprazole: Ulcer healing efficacy and tolerability is similar to omeprazole. It is excreted in urine both as unchanged drug and as sulphone metabolite.

3. Anticholinergics:

a. Pirenzepine: It is M1 selective antagonist, is used in the treatment of peptic ulcer, as it reduces gastric acid secretion and reduces muscle spasm.

b. Propantheline: It is used with other medicine to treat ulcer. It works by slowing the movement of food through the stomach and intestines and decreasing the amount of acid made by the stomach. It has a direct effect on smooth muscles. About 70% drug is excreted in the urine mostly as metabolites.

4. Prostaglandin analogue:

 a. Misoprostol: PGE2 and PGI2 are produced in the gastric mucosa and appear to serve a protective role by inhibiting  acid secretions and inhibits gastrin release, increase mucosal blood flow and have cytoprotective action. Misoprostol is PGE1 analogue.

Pharmacokinetics: Misoprostol is a longer acting synthetic PGE1 derivative which inhibits acid output. Shorter duration of action having very short t1/2. Ulcer healing rates comparable to cimetidine have been obtained in 4-8 weeks, but misoprostol is poorer in releiving ulcer pain.

Side effects: Diarrhea, abdominal cramps, uterine bleeding, abortion.

Uses: Prevention and treatment of NSAID associated gastrointestinal injury and blood loss.

B. Antacids: Antacids are basic substances which neutralise gastric acid and raise pH of gastric contents. Peptic acidity is reduced if pH rises above 4. 

  1. Systemic antacids:

      a. Sodium bicarbonate: It is a potent neutralizer pH may rise above 7. Duration of action is short.

Side effects: Large dose induces alkalosis, ulcer perforation, CHF, edema, acid rebound occurs(due to higher pH more acid is secreted in patients with hyperacidity and duodenal ulcers cause acid rebound).

Uses: Heartburn, to treat acidosis.

 b. Sodium citrate: Similar properties to sodium bicarbonate.

2. Non-systemic Antacids: These are insoluble poorly absorbed basic compounds.

a. Magnesium hydroxide: It reacts with HCL promptly and is an efficacious antacid. It has lower water solubility.

b. Magnesium trisilicate: It has low solubility and reactivity. About 5% of Mg is absorbed systemically. All Mg salts have laxative property.

c. Aluminium hydroxide gel: It is weak and slowly acting antacid. Its 5ml suspension neutralize only 1mEq HCL. The Al3+ ions relax smooth muscle, it delays gastric emptying. It frequently causes constipation  due to its smooth muscle relaxant property.

d. Calcium carbonate: It is potent and rapidly acting acid neutralizer . Ca ions are partly absorbed . It may cause acid rebound. Milk alkali syndrome is a major side effect. Large quantity of milk was prescribed with CaCO3 for peptic ulcer, such regimen may cause syndrome like headache, anorexia, weakness abdominal discomfort.

Antacid combination: A combination of two or more antacids is frequently used:

  1. Fast ( Mag. hydroxide) and slow ( Alum. hydrox) acting components yield sustained effect.
  2. Mag. salts are laxative, while Alum. salts are contipating, combinations may annul each others effect and bowel movement may be least affected.
  3. Gastric emptying is least effected, while alum slats tends to delay it, mag/cal. salts tends to hasten it.                                                          Drug interactions of antacids: By raising gastric pH antacids may reduce the absorption of many drugs, Ketconazole, indomethacin, H2blockers, diazepam, fluoroquinolones, isoniazid and ethambutol.

Uses:  Healing peptic ulcer, GERD, dyspepsia.

  C. Ulcer protectives: 

1. Sucralfate: It is basic aluminium salt of sulfated sucrose. It is strongly adheres to the ulcer base, remain there for 6hrs especially in duodenal ulcer. Surface proteins present at ulcer base starts precipitated together with which it acts as a physical barrier, it prevents acid, pepsin and bile coming in contact with ulcer base.

Pharmacokinetics: Absorbed orally. Healing efficacy is exactly similar to cimetidine.

Side effects: Constipation is recorded in 2%patients. Dry mouth and nausea are infrequent.

Interactions: It Interferes with the absorption of tetracyclines, fluoroquinolones, cimetidine, phenytoin and digoxin.

Uses: Bile reflex, gastritis, prophylaxis of stress ulcers.

b. Colloidal bismuth Subcitrate (CBS): It is a colloidal bismuth compound, water soluble. It heals 60% of  ulcers at 4weeks and 80-90% at 8 weeks. It is also use for gastritis and non ulcer dyspepsia associated with H. pylori.

4. Anti H. pylori drugs: H.pylori is gram negative bacteria survive in hostile enviornment of stomach.

  1. Clarithromycin: The bacteriostatic activity of this antibiotic depends on its capacity to inhibit the protein synthesis by binding to 50s ribosomal subunit.
  2. Metronidazole: Bactericidal activity of metronidazole depends on the reduction of its nitro-groups in anionic radicals, nitroso-derivatives and hydroxylamines  which are able to to damage DNA-helical structure.
  3. Levofloxacin: The use of levofloxacin for H.pylori eradication is increasing worldwide after its major role in ‘rescue therapy’regimens. This drug  exert a dose dependent bactericide effect by binding the subunit A of DNA gyrase an essential enzyme for the maintenance of DNA helical structure .In susceptible strains, levofloxacin stops DNA and at a high doses, even RNA synthesis. When the dose is increased, levofloxacin becomes bacteriostatic agents.
  4. Amoxicillin: Amoxicillin is beta lactam antibiotic. It acts by interfering with the peptidoglycan synthesis, especially by blocking transporters named as penicillin binding proteins(PBP).
  5. Tetracycline: It acts as a bacteriostatic against gram positive and gram negative species by inhibting codon-anticodon link at level of 30S ribosomal subunit and blocking the attachment of aminoacyl-tRNA to the receptor site. It is used in ‘quadruple therapy’.

“Rescue therapy” regimen: Combination of  ” Omeprazole+ Amoxicillin+ Levofloxacin”

“Quadruple therapy” regimen: Combination of  “Omeprazole+ Tetracycline+ Metronidazole”


        1. Which of the following receptor is closed by drugs of peptic ulcer?

a. H1

b. H2

c. Proton pump

d. none

    2. Which of the following drugs are anti histaminics?

a. Cimetidine

b. Omeprazole

c. Pirenzepine

d. Misoprostol

3. Which of the following drugs are anticholinergics?

a. Cimetidine

b. Omeprazole

c. Mg. hydroxide

d. Pirenzepine

    4. Which drug cause acid rebound?

a. Sodium bicarbonate

b. Omeprazole

c. Cimetidine

d. Misoprostol

    5. What are the Risk factor of peptic ulcer?

a. Helicobacter pylori

b. Zollinger-Ellison syndrome

c. a&b

d. None

6. Which ulcers develop sores in the inside lining of the upper portion of small intestine?

a. Gastric ulcers

b. Duodenal ulcers

c. a&b

d. None

     7. Drugs of choice for Zollinger-Ellison syndrome?

a. Antacid

b. H2 antihistamines

c. Proton pump inhibitor

d. Ulcer protectives

      8. In antacid preparation aluminium hydroxide is added with magnesium salts because:

a. Magnesium caused constipation

b. Aluminium caused diarrhea

c. To counteract the laxative effect of alum

d To counteract the constipating effect of aluminium.

9. Select the correct combination of H2 antihistamines, proton pump inhibitors, and anticholinergic drugs.

a. Ranitidine, Pirenzepine, Omeprazole

b. Misoprostol, Pirenzepine, Ranitidine

c. Roxatidine, Esomeprazole, Propanthlene

d. Misoprostol, Famotidine, Rantidine

 10. Which of the following has been associated with peptic ulcer.

a. H. pylori. a gram negative bacteria

b. H. pylori. a gram positive bacteria

c. H. pylori. a gram negative fungi

d. H. pylori. a gram positive fungi

     11. Which of the following correctly defines a peptic ulcer?

a. When lower esophagus gets lined be red colored tissue.

b. A benign lesion of gastric mucosa.

c. When upper esophagus gets lined be red colored tissue.

d. When esophagus starts getting thinner.

     12. Which drugs are used in “rescue therapy” regimen?

a. Omeprazole+ Rantidine+ Ampicillin

b. Tetracycline+ Misoprostol+ Cimetidine

c. Pirenzepine+ Cimetidine+ Misoprostol

d. Omeprazole+ Amoxicillin+ Levofloxacin

13. Which drugs are used in ” quadruple therapy” regimen?

a. Omeprazole+ Amoxicillin+ Levofloxacin

b. Omeprazole+ Tetracycline+ Metronidazole

c. Pirenzepine+ Cimetidine+ Misoprostol

d. Tetracycline+ Misoprostol+ Cimetidine

14. Which of the following drug are ulcer protectives?

a. Sucralfate

b. Omeprazole

c. Misoprostol

d. Cimetidine

15. Which drug posses ” first pass metabolism”?

a. Pantoprazole

b. Roxatidine

c. Cimetidine

d. Tetracycline


  1. b
  2. a
  3. d
  4. a
  5. c
  6. d
  7. c
  8. d
  9. c
  10. a
  11. b
  12. d
  13. b
  14. a
  15. c


  1. “K.D. Tripathi” Page no 695-706, 8th edition 2018.

2. “Khyber medical university” Pharmacology of peptic ulcer, ” Health and medicine”, Jan 18, 2018

3.”Vincezo De Francesco” World Journal of Gastrointestinal pathophysiology.


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