HYPER ACIDITY
Disease hyperacidity is the commonest disease of the fast, fashionable, & fast food based modern life. This is one of the commonest terms also used by the patients to subject each gastric discomfort as hyperacidity. Usually patients having following signs and symptoms are coming with the chief complaint as hyperacidity.
v Heart burn
v Chest pain
v Gastric discomfort
v Abdominal distention
v Sour belching
v Refluxes of the food taken
v Nausea
v Loss of appetite
All these complexes together make the disease hyperacidity. This symptomatology may occur due to many under laying causes they are as discussed below:
General factors :
Vagal effects, hormonal effects insufficient circulation, shock, general ischemia, etc.
Constitutional and Environmental factors :
Age, sex, temperament, family history, social class, geographical distributions and occupation etc.
Local factors related to stomach :
o Aggressive factors :
Hydrochloric acid, pepsin, refluxed bile, NSAIDs, alcohol, pancreatic and proiolytic enzymes, ingested irritants, bacterial toxins, psychological trauma.
o Defensive factors :
Mucus, bicarbonates, blood flow, restitution of epithelium. Thus defensive factors are responsible for the enhancement of mucosal protection. Although no single element may account for mucosal protection, all may be potentially contributing factors. Insight into mucosal protective mechanisms was provided by studies performed by Robert. These studies lead to the introduction of term “Cytoprotection” generally accepted to mean protection of the gastric mucosal by prostaglandins (PGs) against damaging agents.
Role of infection :
Lately some more information has poured in about the prevalence and changing pattern of the disease, the influence of environmental factors and speculation on the role of recently characterized bacterial organisms, Helicobacter pylori, which colonized the gastric mucosa, particularly the antral region.
H. Pylori are a gram-negative spiral bacterium that is found in a patchy distribution overlaying in gastric epithelium. It was formally named as campylobector pylori. At present 9 species of Helicobacter genus are available and all excluding H. plyori, are of animal origin. H. Felis can be introduced into mice to produce intense colonization and inflammation of stomach.
H. pylori organisms have strong capability of urease production. The bacteria then split urea and the ammonia thus released may become cause of increased acidity and hence enabling organism to survive. The released ammonia may also be cytotoxic.
H. pylori have been implicated in the etiology of belching, indigestion and chronic peptic ulceration. H. pylori induced gastritis present in about 60% of patient with gastric ulcer. Until recently pathogenesis of gastric and duodenal ulcers has been attributed to an imbalance between aggressive factors such as acid and pepsin that damage the gastric mucosa and protective factors such as prostaglandins that prevent the damage. Recent evidences relate H. pylori to the pathogenesis of chronic duodenal ulcer as H. pylori infection and antral gastritis are found together in more than 95% of patients with duodenal ulcers.
Pathogenesis :
Following factors are important in development of Hyperacidity:
1) Luminal acid and pepsin are requisite.
2) Increased mucosal tissue acidosis with subsequent decrease secretion of bicarbonate (The alkaline ‘tide’).
3) Reduced mucosal blood flow, whatever its basis (Shock, Drugs, Stress) causing hypoxic injury & impairing the secretion of bicarbonate.
4) Disruption of the mucosal barrier (i.e. the intake layer of surface mucosal epithelial cells) permitting back diffusion of hydrogen ions and in turn increased shedding of surface of cell.
Ayurvedic Treatment :
· Indukantam kasayam 15ml added with 45 ml hot water and to be taken at morning empty stomach & evening 5pm
· Dhanwantaram tab 1 before lunch and dinner
· Ashtachurnam 1 teaspoon with hot water before breakfast
· Amalaka rasayanam 1 table spoon at bed time followed by hot milk
