The tummy is a J-shaped expansion of the GI piece of land merely lies below the stop ; the digestive tubing dilates into an elongated pouchlike construction, the size of which varies harmonizing to several factors, notably the sum of dilatation. For sometime after a repast, the tummy is enlarged because of dilatation of its walls, but, as nutrient foliages, the walls partly collapse, go forthing the organ about the size of a big sausage. In grownups the tummy normally holds a volume upto 1.0 to 1.5L.

The fundus, organic structure and the pylorus are the three divisions of the tummy. The fundus is the enlargement part of the left and above gap of the gorge into the tummy. The organic structure is the cardinal portion of the tummy, and the pylorus is its lower part.

1.1.2 Curves of the tummy:

The curve formed by the upper right surface of the tummy is known as the lesser curvature ; the curve formed by the lower left surface is known as the greater curvature.

1.1.3 Sphincter musculuss:

Sphincter muscles guard both tummy gaps. A sphincter musculus consists of round fibers so arranged that there is an gap in the Centre of them ( like the hole in a ring ) when they are relaxed and no gap when they are contracted.

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The cardiac sphincter controls the gap of the gorge into the tummy, and the pyloric sphincter controls the gap from the pyloric part of the tummy into the first portion of the little bowel.

1.1.4 Stomach wall:

Gastric mucous membrane

The epithelial liner of the tummy is thrown into creases, called rugae, and marked by depressions called stomachic cavities. Numerous coiled tubular- type secretory organs, stomachic secretory organs, are found below the degree of the cavities, peculiarly in the fundus and organic structure of the tummy. The secretory organs secrete most of the stomachic juice, a mucose fluid incorporating digestive enzymes and hydrochloric acid.

1.1.5 Functions of the tummy:

The tummy carries on the following the maps:

It serves as a reservoir, hive awaying nutrient until it can be partly digested and moved farther along the GI piece of land.

It secretes stomachic juice, incorporating acid and enzymes, to assistance in the digestion of nutrient.

It carries on the limited sum of soaking up – of some H2O, intoxicant, and certain drugs.

It produces the endocrine gastrin, which help ordinance of digestive maps.

It helps to protect the organic structure by destructing infective bacteriums swallowed with nutrient or with mucose from the respiratory piece of land.

1.2 Regulation of stomachic acerb secernment:

HCL-release

1.2.1 Phases of secernment of stomachic juice ( Kathleen, et. al. , 1996 )

There is ever a little measure of stomachic juice nowadays in the tummy, even when it contains no nutrient. This is known as fasting juice. Secretion reaches its maximal degree about 1 hr after a repast, so declines to the fasting degree after about 4 hours. During a repast, secernment of stomachic juices ( incorporating HCl and pepsinogen ) increases from a few milliliter / hr ( the usual values between repasts ) to about 1.5 L. HCl and pepsinogen. Gastric secernment occurs in three stages:

a. Cephalic stage, b. Gastric stage, c. Intestinal stage

a. Cephalic Phase ( outputs about 1/5 of entire secernment )

A psychological stimulation ( such as expecting a repast, its odor, sight and texture ) starts stomachic secernment before nutrient reaches the tummy. This flow of juice occurs before nutrient reaches the tummy and it is because of automatic stimulation of the vagus nervousnesss initiated by the sight, smell or gustatory sensation of nutrient. When the pneumogastric nervousnesss have been cut ( vagotomy ) this stage of stomachic secernment Michigans.

b. Gastric Phase

The presence of partly digested nutrient ( particularly peptides and aminic acids ) in the tummy promotes the secernment of the endocrine gastrin. This peptide endocrine acts on the tummy, thereby exciting secernment. Histamine and acetylcholine besides stimulate secernment, and all three factors act synergistically, so that their entire potentiating consequence is markedly higher than the amount of their single parts. Therefore, barricading anyone of these factors is adequate to arouse a significant lessening in secernment. Gastrin besides increases stomachic motility, taking to motion of the tummy contents ( chyme ) from the tummy and into the duodenum. Gastric stage secernment is suppressed when the pH in the pyloric antrum falls to about 1.5.

c. Intestinal Phase or Enteric Phase

When the partly digested contents of the tummy reach the little bowel, a endocrine complex enterogastrone, ( Enterogastrone has been described as any endocrine or combination of endocrines released by the bowel that inhibits stomachic secernment ) is produced which slows down the secernment of stomachic juice and reduces stomachic motility. Two endocrines organizing this composite are secretin and cholechystokinin ( CCK ) . By decelerating the emptying rate of the tummy, the contents of the duodenum go more thoroughly assorted with gall and pancreatic juice. This stage of stomachic secernment is most pronounced when the repast has had a high fat content.

CONTROL OF GASTRIC ACID IN STOMACH:

hcl control

Figure1: It shows the control of release of stomachic acid in the tummy by moving through the histamine, prostaglandin, acetylcholine and gastrin receptors.

1.3 Peptic Ulcer

Peptic ulcers disease refers to a group of upsets characterized by limited lesions of the mucous membrane of the upper GI piece of land ( particularly of the tummy and duodenum ) . The lesions occur in parts exposed to stomachic juices. When the tummy ‘s natural protections from acerb halt working ulcers will happen. Duodenal ulcers about ever develop in the duodenal bulb ( the first few centimeters of the duodenum ) . A few, nevertheless, arise between the bulb and the ampulla. Gastric ulcers form most normally in the antrum or at the antral-fundal junction. About 80 % of peptic ulcers are duodenal the others are stomachic ulcers. Most duodenal ulcers appear in people between ages 20 and 50 old ages, while stomachic ulcer normally occurs between ages 45 and 55 old ages. Duodenal ulcer is twice every bit common in work forces as in adult females and stomachic ulcers affect work forces and adult females every bit. Approximately 10 to 20 % of stomachic ulcer patients besides have a coincident duodenal ulcer.

peptic ulcer

Gastric ulcer is frequently a chronic disease and may prevail for 10 to 20 old ages characterized by perennial episodes of mending and re-exacerbation. Peptic ulcers occur when there is an instability between violative factors and defensive mucosal factors ( Goel and Bhattacharya, 1991 ) . Ulcer in the mucous membrane can be because of either dislocation of mucous membrane with the development of surface defects or failure of damages of mucosal unity ensuing in deceleration or failure of healing of the ulcers. No evident causal factor is sufficiently unambiguously associated with peptic ulcers to justify univocal deduction in pathogenesis of the ulceration. The defence mechanism of the GI mucous membrane against aggressive factors, such as hydrochloric acid, bile acid, free groups, Helicobacter pylori colonisation, non-steroidal anti-inflammatory drugs, etc. , chiefly consists of functional, humoral and neural factors. Mucus-alkaline secernment, mucosal microcirculation, cellular mucous secretion, life span of mucosal cells and motility act as functional factors, while prostaglandins and azotic oxide act as humoral factors, and capsaicin sensitive centripetal nerve cells act as neural factors. All the above factors are known to lend to mucosal protection ( Tsukimi and Okabe, 2001 ) .

The precise biochemical alterations during ulcer coevals are non clear yet, although assorted hypotheses have been proposed from clip to clip. Increased stomachic motility, vagal over activity, mast cell degranulation decreased stomachic mucosal blood flow and reduced prostaglandin degree during stress status is thought to be involved in ulcer coevals. Similarly function of O derived free groups have been shown to play a function in experimental stomachic harm induced by ischaemia and reperfusion, hemorrhagic daze and ethanol disposal. Helicobacter pylori a pathogen is now known to be the most common and of import causes of stomachic ulcer in worlds ( Davies et al. , 1994 ) , exhibits active redness with epithelial harm accompanied by neutrophil migration.

Although the presently used drugs for ulceration are loosely classified into two, those that lessening or counter addition in acid-pepsin secernment and those that afford cytoprotection by virtuousness of their effects on mucosal defensive factors. Ulcer therapy is now chiefly focused on restricting the hurtful effects of violative acid secernment. Since stomachic acid is one of the major aggressive factor lending to peptic ulcer disease, the decrease of stomachic acid either by surgical or pharmacological intercession has been used to advance ulcer healing. However, non all patients, with stomachic or duodenal ulcer have high acid secernment. In fact, merely 30 % -40 % of instances with duodenal ulcer have hypersecretion of stomachic acid and, in patients with stomachic ulcer, acerb secernment is either normal or low ( Gupta et al. , 1980 ) . In these instances, decreased mucosal opposition might be the dominant factor.

The neutralisation of stomachic acid can be done by antacid disposal, but their effectivity is merely for a brief period. Muscarinic adversaries such as pirenzepine or telenzepine are effectual inhibitors of acerb production. The histamine H2-receptor adversaries ( H2RA ) like Tagamet, Zantac, famotidine etc. act as powerful inhibitors of acerb secernment. Complete suppression of parietal cells acerb secernment by receptor adversary is hard because of complexness of known receptors on parietal cells and a assortment of 2nd courier signaling system coupled to these receptors, which involve adenylate cyclase coupled with histamine receptor and intracellular Ca+2 with acetylcholine receptors. Therefore, the most successful and desirable therapy is to suppress the enzyme responsible for acerb secernment. Furthermore, H2RA have been reported to hold some inauspicious reactions runing from stomachic carcinoid to tolerance and recoil acid secernment. Inhibition of stomachic H+/K+ -ATPase of the parietal cell by drugs such as by proton pump inhibitors ( PPIs ) like Prilosec, Prevacid, timoprazole, etc. has been shown to be effectual in the intervention of peptic ulcer disease. However, such agents irreversibly inactivate the ATPase and the return of acerb secernment following such inhibition requires de novo synthesis of new pump.

Although these drugs have brought about singular alterations in ulcer therapy, the efficiency of these drugs is still problematic. Reports on clinical rating of these drugs shows that there are incidences of backslidings and inauspicious effects and danger of drug interactions during ulcer therapy. Further, in the development states, like India, most of the population is populating in rural countries and depending on their autochthonal system of drugs because of expensive modern intervention. Hence, the hunt for an ideal anti-ulcer drug continues and has besides been extended to herbal drugs in hunt for new and fresh molecules, which afford better protection, diminish the incidence of backsliding and diminish the cost of the intervention.

Of late the hunt for new safe alternate drugs have rekindled the involvement in cytoprotective drugs, which protect the stomachic mucous membrane from damaging agents without act uponing acerb secernment or neutralizing intragastric sourness. Cytoprotection has been defined as the ability of pharmacological agents-originally prostaglandins to forestall or cut down stomachic, duodenal, or enteric mucosal hurt by mechanisms other than suppression of stomachic acerb secernment. Although few drugs like Carafate and prostaglandin parallels are recognized as cytoprotective agents ( Vergin and Kori-Lindner, 1990 ) , many natural drugs have been reported to posses this activity viz. plantain banana ( Musa sapientum volt-ampere Paradisiaca ) , Tectona grandis, Azadirachta indica and rasayana drugs like Centella asiatica, Asparagus racemosus, Convolvulus pluricaulis, Emblica officinalis, Bacopa monniera and Withania somnifera, etc. ( Goel and Sairam, 2002 ) .

India is one of the state rich in medicative workss which were used by our ascendants. Traditionally, workss were used as medical specialty in traditional manner such as Ayurveda, Naturopathy, Siddha and Unani. After cognizing the used of workss in medical specialty, man-made drugs were now started replacement by herbal merchandises.

Worlds have used works stuffs since prehistoric times and in some states such as China documental grounds shows that herbal medical specialties have been used for at least 7000 old ages. In Europe there is a rich history in the usage of herbal medical specialties and these have been good documented in mediaeval herb teas such as Culpeper ‘s and Gerard ‘s materia medica. Nowadays many states are holding involvement in utilizing Indian medicative workss as it can bring around many diseases and other intents.

Herbal medical specialties differ from man-made drugs in several properties. Though, herbal medical specialties are assorted chemical compounds, all have non been isolated, characterized and quantified. When an infusion of a works or a compound isolated from the works has to be clinically evaluated for a curative consequence non originally described in the texts of traditional systems or, the method of readying is different, it has to be treated as a new substances or new chemical entity. The same type of ague, subacute and chronic toxicity informations has to be generated.

Majority of medicative herbs contain tonss of different compounds, frequently of great complexness, flavonoids, saponins, glycosides, alkaloids, mucilage, tannic acids, polyoses, etc. , that buffer, modulates and modify the consequence of any “ active rules ” . Study after survey has shown that administrating of stray purified components of the whole or portion of the works can non mime effects produced by infusions of same portion of the works.

1.3.1 Pathophysiology of Peptic Ulcer

Peptic ulcer by and large occurs when there is an instability between Aggressive stomachic factors ( acid, pepsin, Helicobacter pylori, refluxed Bile salts ) and defensive mucosal factors ( stomachic mucosal barrier, Bicarbonate secernment, rapid cell turnover, high blood flow ) ( Goel & A ; Bhattacharya, 1991 ) . The intervention of peptic ulcer is directed against Reduction of aggressive factors or sweetening of mucosal defence of Stomach and duodenum with cytoprotective agents.

H. Pylori

H.Pyloric is a Gram -ve spiral-shaped bacteria. H.Pyloric is the most common cause of non-NASID associated peptic ulcer disease. H.Pyloric has been found in the stomachic antrum of a important figure of patients with duodenal ulcers and stomachic ulcers.

H.Pyloric lives in the acidic environment of the tummy. The initial infection is transmitted by the unwritten path. H.Pyloric attaches to adhesion molecules on the surface of stomachic epithelial cells. In the doudenum, H.Pyloric attaches merely to countries incorporating stomachic epithelial cell that have arisen as a consequence of surplus and harm to the duodenal mucous membrane. H.Pyloric is able to populate in such a hostile environment partially because of its production of the enzyme addition, which converts carbamide to ammonia. The ammonium hydroxide buffers the H+ and signifiers ammonia OH making an alkalic cloud around the bacterium and protecting it from the acidic environment of tummy. It causes redness and epithelial cell harm ( Golan, and Arman ) .

Nonsteroidal anti-inflammatories

More than 100, 000 patients are hospitalised each twelvemonth for NSAID-associated gastro-intestinal complications and GI hemorrhage has a 5 % to 10 % mortality rate in these patients.

NSAID-associated GI harm is attributable to both topical hurt and systemise effects of the NSAID. Most NSAIDS are weak organic acids. In the acidic environment of the tummy, these drugs are impersonal constituents that can traverse the plasma membrane and enter stomachic epithelial cells. In the impersonal intracellular environment, the drugs are recognized and trapped. The ensuing intracellular harm is responsible for the local GI hurt associated with NSAID usage.

Gastric acid secernment

Inhibition of cycloxygenase prostaglandins Bicarbonate/ Mucous

Production

Blood flow

Nonsteroidal anti-inflammatory

Neutrophil attachment Mucosal dama-

Expression of intercellular vascular endothelial Ge due to neutro-

Adhesion molecules in stomachic cells phil free groups

Vascular endothelium and peptidases.

Acid hypersecretion

Acid hypersection is an of import causative factor in some patients with peptic ulcer disease. Zollinger-Ellison Syndrome ( Z-E-S ) are two clinical illustrations in which hyperacidity leads to peptic ulcer disease. In Z-E-S, a gastrin-recreting tumour of the non-beta cells of the endrocrine pancrease lead to increased acerb secernment. In craving ulcer, seen in patients with rearward caput hurts, heightened vagaltone causes stomachic hyperacidity.

Table: 1. Aggravating and Defensive Factors in Stomach

( Anoop & A ; Jegadeesan, 2003 ) .

Aggravting factors

Defensive factors

Gastric sourness

Gastric mucosal secernment

Peptic enzymes, histamine, acetylcholine, 5-hydroxytryptamine

Bicarbonate secernment into mucose

NSAIDS, Steroid, Fe2+ salt, Erythrocin, anticancer drugs

Mucosal blood flow

Smoking

Apical surface membrane conveyance

Alcohol

Epithelial regenerative capacity

Rapid stomachic voidance

Amplification of prostaglandins

Duodenal gastric reflux

Ischemia daze

Helicobacter pylori

Delayed gastric emptying

Gastric mucosal ischaemia

Burn, intracranial surgery, injury, emphasis

Figure 2. Physiological and Pharmacological Regulation of Gastric Secretion: The Basis for Therapy of Acid-Peptic Disorders. ( Goodman and Gillman, 622 ) .

Qip – ela1

Figure is demoing the interactions among an enterochromaffin-like ( ECL ) cell that secretes histamine, a parietal cell that secretes acid, and a superficial epithelial cell that secretes cytoprotective mucous secretion and hydrogen carbonate. Physiological tracts, shown in solid black, may be stimulatory ( + ) or inhibitory ( – ) . 1 and 3 indicate possible inputs from postganglionic cholinergic fibers, while 2 shows nervous input from the pneumogastric nervus. Physiological agonists and their several membrane receptors include: acetylcholine ( ACh ) , muscarinic ( M ) , and nicotinic ( N ) receptors ; gastrin, cholecystokinin receptor 2 ( CCK2 ) ; histamine ( HIST ) , H2 receptor ; and prostaglandin E2 ( PGE2 ) , EP3 receptor. Drug actions are indicated by dotted lines. A bluish X indicates marks of pharmacological hostility. A light blue dashed arrow indicates a drug action that mimics or enhances a physiological tract. Shown in blue are drugs used to handle acid-peptic upsets. NSAIDs are nonsteroidal anti-inflammatory drugs and are ulcerogenic.

1.4 Gastrointestinal Motility:

Laxatives are drugs that either accelerate fecal transition or diminish fecal consistence. They work by advancing one or more of the mechanisms that cause diarrhea. Because of the broad handiness and selling of OTC laxatives, there is a possible that an appropriate diagnosing will non be sought ( Jahangir moini ) .

Rarely in medical specialty is there an absolute indicant for the usage of laxatives. A high fiber, good balanced diet rich in fruits and veggies supplemented by bran should be adequate to normalise intestine map. The fright of autointoxication and the changeless concern of many patients sing the frequence and quality of intestine motion make laxatives one of the most popular over – the – counter drugs in the market with serious potency for user maltreatment. Accepted indicants for laxatives and stool softners include readying for diagnostic colonic scrutiny ( Barium enema, colonoscopy: intervention of anorectal upsets ) and bar of hepatic brain disorder ( Smith and Reynard ) .

Fibre is defined as the undigested residue of fruits, veggies, and other nutrients of works beginning after digestion by the human GI enzymes. Fibre ‘s H2O keeping capacity is the ability of fiber to keep H2O and do bulking of fecal stuffs possible. Fibre ‘s stool bulking capacity is the ability of the fiber to increase the volume of enteric content because it can absorb and holds H2O. Bacterial growing in the colon provides extra bulking. Insoluble fiber ‘s velocities GI theodolite clip.

Cholinergic mechanisms are besides responsible for modulating motor phenomena in the intestine ; therefore it is non surprising that cholinomimetic agents are effectual in advancing GI motility. It besides has cholinomimetic belongingss, seemingly sensitising enteric smooth musculus cells to the action of Acetylcholine instead than moving on acetylcholine receptors. The drugs acts to rush esophageal clearance, raise lower esophageal sphincter force per unit area, accelerate gastric voidance, and shorten little intestine theodolite clip

1.4.1 Mechanism of Laxative Action: ( KD Tripathi, 1999 )

a. By their hydrophilic or osmotic nature, laxative can do keeping of fluids, in the colonic content, every bit good as addition the mass.

b. Inhibiting Na+K+ATPase of villous cells – impairing electrolyte and H2O soaking up.

c. Stimulating adenyl cyclase in crypt cells – increasing H2O and electrolyte secernment.

d. Enhancing PG synthesis in mucous membrane which increases secernment.

e. Structural hurt to the absorbing enteric mucosal cells.

1.4.2 Categorization of Laxatives: –

Many drugs in low doses act as laxative and in larger doses as cathartics

1. Bulk organizing 4. Stimulant cathartics

Dietary fiber: Bran ( a ) Diphenylmethanes

Fleawort Phenolphthalein

Methycellulose 5. Anthraquinones

2. Stool softner Senna, Cascara sagrada

Docusates ( DOSS ) 6. Osmotic cathartics

3. Lubricant Magnesium, Na salts

Liquid paraffin Lactulose

1.4.3 Anthraquinone Derived functions: –

Senna is obtained from the foliages and cods of Cassia augustifolia and contains the anthraquinone glycosides called emodins. In unwritten dose the sennosides is ill absorbed, but after remotion of the sugar and decrease to anthrol by colonic bacteriums, they are absorbed into circulation – excreted in gall to move on little bowel. It takes 6-7 hour to bring forth action. The active rule is believed to move on the myentric rete to increase vermiculation and lessening cleavage. They besides inhibit salt and H2O soaking up in the colon. In India, sennosides are normally marketed in combination with stool softeners such as docusates. . Side effects observed are nausea, purging, diarrhea, gripes, urine stain ( xanthous brown to red ) and melanism ( colonic atonicity and mucosal pigmentation after a regular usage of the drug ) . It should be used carefully in adult females and kids bellow 6 old ages of age, and after abdominal surgery.

Preparations

GLAXENNA check. Sennosides ( Ca salt )

11.5 milligram.

SOFSENA tab – 12 milligram.

PURSENNID check -18 milligram

LAXSENA tab – 12mg, 18mg ( strong suit )

x

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