Anti ulcer drugs

Anti ulcer drugs

Anti ulcer drugs are used for prevent and treat ulcer formation in the gastro intestinal tract.

Before going through anti ulcer drugs, have a look of parietal cell and basic physiology of HCl secretion.

Parietal cell structure with receptors activity - Anti ulcer drugs
Parietal cell structure with receptors activity

Ulcers

Factors that play a role in peptic ulcer (gastric and duodenal ulcers) formation is known as ulcerogenic factors, these are listed here-

  1. Acid hypersecretion
  2. pepsin
  3. Drugs (NSAIDs, corticosteroids, ethanol, chemotherapeutic agents, cigarettes)
  4. Infection
  5. Tumors
  6. Stress – head trauma, shock/sepsis, emotional
  7. Alteration of protective factors
  8. Disruption of mucosal integrity and
  9. Decreased bicarbonate secretion

Symptoms of ulcers are due to a combined effect of hydrochloric acid and pepsin. Acid causes pain but not tissue damage but pepsin, which is activated in acid environment, digests mucosal, muscular and vascular layers of stomach & intestines.

Alkaline reflux from intestines may inflame gastric mucosa also.

Gastric (stomach) ulcers are not due to too much acid but Duodenal (intestinal) ulcers are due to increased acid secretion in stomach.

When stomach empties into intestines there is too much acid for pancreatic secretions to neutralize and this acid erodes tissues.

Most common causes of ulcer are H. pylori and NSAIDs as well as gastrin hypersecretion.

Goals of drug therapy for ulcers

  1. Neutralize existing gastric acid – antacids can be used
  2. inhibit acid secretion – H2 antagonists, proton pump inhibitors can be used
  3. treat infection (H. pylori) – antibiotics can be used
  4. protect ulcer from further damage – sucralfate

Anti ulcer drugs

1. Antacids

Antacids are agents which neutralize excess acid. Some of the commonly used antacids include sodium bicarbonate, aluminium hydroxide and dihydroxy-aluminiumcalcium carbonate and magnesium hydroxide.

The weak base reacts with the gastric hydrochloric acid to form a salt and water. this reaction causes an increase in the gastric pH. but rebound acidity is still problem with antacid use.

The potency of antacids is generally expressed in term of ‘Acid neutralizing capacity / ANC‘.

Sodium bicarbonate

Sodium bicarbonate has a rapid onset of action. But it is not an ideal antacid due to the rebound acidity. (stimulation of acid production once the pH exceeds 4, due to gastrin secretion)

As sodium bicarbonate is readily absorbed into systemic circulation, it alters systemic pH and produces electrolyte disturbances. This in turn may lead to edema, hypertension or heart failure.

Aluminum hydroxide

The insoluble aluminum chloride that is formed due to the reaction of hydrochloric acid and aluminium hydroxide often causes constipation. It also binds with tetracycline to inhibit its absorption.

Calcium carbonate

The absorption of ~10% of calcium chloride may result in hypercalcemia (muscle weakness, kidney stone formation) and rebound gastric acidity. Constipation may occur with high doses.

Magnesium hydroxide

Magnesium hydroxide causes prolonged neutralizing effect due to slow stomach emptying. Poor absorption of magnesium salts may result in diarrhoea. Combinations of aluminum or calcium containing antacids with magnesium containing antacids can nullify the adverse effects on bowel function.

2. Histamine H2 receptor antagonists

Endogenous histamine released from enterochromaffin-like cells or mast cells stimulates parietal H2 receptors. Histamine activates a cyclic AMP pathway, activates H+_ K+-ATPase and leads to increased H+ in gastric lumen. H2 receptor antagonists can block this histamine induced secretion and are helpful reducing the acid secretion during ulcers.

Examples of H2 receptor antagonists include cimetidine, ranitidine, famotidine, nizatidine, Roxatidine etc.

In general, these drugs are well tolerated with few side effects (less than 3% with cimetidine and <1% with other drugs).

Cimetidine

Cimetidine exhibits antiandrogenic properties leading to decreased sperm count, gynecomastia and also inhibits hepatic drug metabolism. Inhibition of cytochrome P450 activity by cimetidine leads to potential drug interactions. This feature is not seen with ranitidine, famotidine and nizatidine.

Ranitidine

Ranitidine is 5 times more potent then cimetidine (Longer duration of action with 24 hours acid suppression is obtained clinically because of high potency). Ranitidine also have Prokinetic activity along with no antiandrogenic action.

3. Proton pump inhibitors

Proton pump inhibitors are also called as acid blockers. Examples of proton pump inhibitor drugs are omeprazole, lansoprazole, pantoprazole.

These drugs irreversibly inhibit K+H+-ATPase proton pump in gastrointestinal parietal cells i.e. inhibits entry of H+ ion entry into lumen.

PPI drugs also appear to have antimicrobial activity against H. pylori.

Note

Proton pump inhibitors break down in the acid environment of the stomach and must be given orally as enteric coated preparations (Pantoprazole also available in injection for i/v) and they have short plasma half-lives but are long acting.

Proton pump inhibitors inhibit hepatic drug metabolism and are very well tolerated. These drugs heal duodenal ulcers more rapidly than H2 antagonists.

They are used primarily for ulcers refractory to other treatments and are also used for reflux esophagitis and management of gastrinomas.

4. Cytoprotective drugs / PG analog

Misoprostol, an analogue of prostaglandin (PGE1) analog is used as a cytoprotective drug. Prostaglandins (membrane derived second messengers) have protective actions on gastric mucosa.

They increase mucosa formation and increases release of bicarbonate (HCO3). Adverse effects are not common except diarrhoea and abdominal cramping.

As this drug may cause abortion, it is not recommended for use in pregnant animals. It is used for short-term management of peptic ulcers and also to reduce gastrointestinal irritation associated with NSAID (aspirin-like drugs) therapy.

Drugs for eradication of Helicobacter pylori bacteria

1. Multiple antibiotics (metronidazole + amoxicillin or tetracycline or clarithromycin)

2. Bismuth subsalicylate

3. Most effective treatment is a combination of multiple antibiotics with H2 antagonist or proton pump inhibitor for 6 months

5. Sucralfate

Sucralfate is a complex of sulfated sucrose and aluminum hydroxide and is known as gastric band aid. Sucralfate polymerizes to a viscous gel at a pH less than 4. It combines with proteins and adheres to ulcer forming a barrier resistant to acid and pepsin and binds to bile salts which are implicated in ulcer pathogenesis.

It is as effective as cimetidine or antacids at healing peptic ulcers and is useful in treating gastric reflux. It is a Gastric protective drug.

Use of Sucralfate: Sucralfate is used in the treatment of gastric and duodenal ulcers in dogs, cats and foals.

Adverse effect of Sucralfate: Constipation may occur with long term therapy.

Drug Interactions of sucralfate: It interacts with many drugs and shown to interfere with absorption of tetracyclines, fluoroquinolones, cimetidine, phenytoin and digoxin.

6. Anticholinergic drugs

Atropine drug reduce the volume of gastric juice without changing pH but produce intolerance side effect. Pirenzepine is a selective M1 anticholinergic which reduce gastric secretion by 40 to 50% without intolerable side effect.

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