Drakshyadi gutika in amlapitta kc
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Drakshyadi gutika in amlapitta kc



To study the efficacy of Drakshyadi Gutika in Amlapitta

To study the efficacy of Drakshyadi Gutika in Amlapitta



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Drakshyadi gutika in amlapitta kc Drakshyadi gutika in amlapitta kc Document Transcript

  • INTRODUCTION Today’s life style is completely changed by all the means ourdiet pattern, life styles and behavioral pattern is changed & it is notsuitable for our normal physiology of digestion of body & all abovementioned causes aggravated dosha which creat agnimandya & dueto improperly it metabolized it get convert into shukata (vitiatedliquid acid) & this gets situated in Amahsaya which is called asAmlapitta1. In recent years there has been an unprecedented increase ofincidences related to GI system due to changing in life style. Dietpattern, behavioral pattern & mental stress & strain. Amlapitta is a such type of GI disorder due to same causativefactor as above described in Ayurvedic parlance, closely resembleswith Gastritis in modern science also and in chronic stage it maylead to ulceration condition. Charak & Kashyapa have clearly indicated that the GrahaniDosha & Amlapitta occur in the persons who could not check thetemptation of food. Ajirna ofter encountering the specific Doshas &affinity with specific site may cause various diseases. Annavishaproduces due to Ajirna when mixed with pittadi Dosha & lodges inAmashaya then it produces the Amlapittadi diseases. The first & foremost task in Ayurvedic disease management isa proper understanding & description of its etiopathogenesis. In thisrespect Acharya Charaka has told that Agni is responsible for Ayu,Varna, Bala, Swasthya. Utsaha, Upachaya, Prabha, Ojo & Teja & italso gives the importance as long life in the functioning state2 &even death in unfunctioning state of Agni also Acharya Charaka3. & 1   
  • Acharya Vagbhata has clearly defined the role of Agni in theetiopathogenesis of all the human ailments4. Charak has explained the sequential progression of diseasesof G.I.T. to which Sanghara Granthakara has given a separatedisease status. In samhita Amlapitta is no mentioned as a separatedisease entity but there are several references in charaka samhitaregarding Amlapitta. The terminology has been used at 9 places.From the references it gives a clear cut idea of Nidana Panchaka &management in his period. Acharya kashapa was the first who gives detail description ofthe disease5. And analyzed first it only Doshik basis, where asmadhavakara gives status to the disease and he further classified iton according to Gati i.e. Urdhvaga Amlapitta & Adhoga Amlapitta aswell as on Doshika basis6. Acharya Kashapa belived that the disease is caused byvitiation of Doshas (Tridosha) causing mandagni leading tovidagdhajirna manifesting as Amlapitta. Madhavakara following Charaka has described thedevelopment of Amlapitta due to Vitiation of pitta which is alreadyincreased due to its own causes. This disorder is the result ofGrahani Dosha. Gastritis & non-ulcer dyspepsia have been co-related withAmlapitta by several MD & Ph. D. Scholars of Ayurveda. As perModern interpretation the symptoms of Amlapitta found in certainpathophysiological condition of GI such as hyperacidity with occur inAPD diseases7. 2   
  • Modern medicine is not having proper medication for gastricdyspepsia. Ayurveda has a lot to offer in this regard. Ayurvedicphysicions are providing cure for the patients of these chronicdyspeptic disorders. Several single & compound drug has been tried in thisdisease. Acharyas told to use the drugs which are having Tikta-Madhura rasa. Madhura Vipaka Sheeta Virya & Laghu Rukshaproperty with kapha-Pittahara action. Taking all these points into consideration the study wasplanned to evaluate aims & objectives. 3   
  • AIM & OBJECTIVES1. To study the efficacy of ‘Drakshyadi Gutika’ in Amlapitta.2. To evaluate clinical effect of ‘Drakshyadi Gutika’ in the management of Amlapitta.3. To study the etiopathogenesis of Amlapitta according to Ayurvedic text as well as modern science.4. To study side effects of ‘Drakshyadi Gutika’ if any. 4   
  • BRIEF REVIEW OF ANNAVAHA SROTASA ANATOMICAL & PHYSIOLOGICAL ASPECTS.DEFINATION :- The word Annavaha srotasa means the channel through whichfood is transported. The functions of organs of ANNAVAHA SROTAS(Alimentary system) concerned with ANNA ADANA (ingestion offood), ANNA PACHANA (digestion) SARA KITTA VIVECHANA(Separation of nutrient and waste portions) and RASA SOSHANA(Absorption of nutrients)MOOLA 8 :- According to Charaka - Amashya & vamparshva According tosushruta - Amashaya & Annavahi Dhamanyas. Charaka has saidthat Amashaya and vamparshva are the Moola of Annavaha srotasa.Acharya Sushruta has said that Amashaya and AnnavahiDhamanyas are the Moola of Annavaha srotasa. Chakapani hasgiven two terminologies - Urdhva and Adho for Amashya. UrdhvaAmashaya was the place of kapha while Adho Amashaya was thepalce of pitta. The deglutination and ingestion process of food isstart from mouth and in upper part of the stomach. main digestiveprocess is start from stomach. Digestive juices secreat from lowerpart of the stomach and intestine Bile and panereatic juices secretfrom liver and pancreas than after come into the small intestine.Therefore we can include oesophagus and upper part of thestomach in Urdhva Amashaya and lower part of the stomach &small intestine in Adho Amashaya. The term Annavahi Dhamanyasare also a Moola of Annavaha srotasa. It means the channels whichtransplant the end products of Anna from the intestine to theplasma blood. Under the microscope the mucous membrance of thesmall intestine contains millions of finger like projections known as 5   
  • villia. This villus is lined by a single layer of epithelial cells and smallarteries, veins and lymphatic vessels. In function, the villi act as asemi permeasble membrane and permit the passage of digestedfood through the Rasavaha and Raktavaha srotansi contained intheir. In other words, these microscopic parts of the membranecarry out the transportation of the Anna Rasa though the intestinalbarrier.Pittadhara Kala:- Acharya Sushruta & vagbhatta both have described pittadharakala. Acharya Sushruta say "THe sixth Kala situated betweenPakvashaya and Amashaya is the pittadhara kala and it is known asGrahani. In his view, "The intrgity of Grahani depends upon Agni9."In charaks opinion "Grahani is so called beacuse it receives andretains the food for the duration of its digestion. He observed thatthe food, which has reached the Amashaya after under goingdigestion absorbed." Pittadhara kala is provides the digestive juicescollectively termed as Pachakagni or Jatharagni. These juices notonly digest the food but also aid the sepration of the sara from thekittabhaga10. (Sara kitta vibhajana kriya) The description ofpittadhara Kala shows that it is a macroscopic structure which notonly serves as a protective lining of the small intestine membrane,but also as a secreting and absorbing structure.Samana Vayu11 :- Vagbhatta said that Samana Vayu is present near the Agniand responsible for the reception, digestion, separation andpropulsion of the food. The Samana Vayu function are similar tointrinsic nervous system of the stomach and intestine. This systemis related to brain and spinal cord. The peristaltic movement ofintestine are responsible for mechanically breakdowns intestinalcontents and throughly mixed up with the juice of pancreas liver 6   
  • and intestine. They absorbed through the intestinal wall. This hasbeen described the function of Samana Vayu as digestion of food,separation of nutrients fraction of food and expulsion of undigestedfood. (Annapachana, Vivechana and Munchana.) So, as anAnatomical view, we can consider fallowing orgens & systems inAnnavaha srotasa.(A) Amashaya :-(i) Urdhava :- (a) Oesophagus (b) Upper part of the stomach(ii) Adho:- (a) Lowerpart of the stomach (b) Small intestine(B) Pittadhara kala:- Innner Laner of mucous membrance of thesmall intestine and lower part of the stomach also.(C) Annavali Dhamanyas:- The channels that receives the endparticlesof the food from the intestine.(D) Samana Vayu:- Intrinsic nervous system of the stomach &small intestine.AHARA PAKA KRIYA:-The Ahara undergoes two preoceses for complete digestion.(A) Avasthapaka(B) Vipaka In Ayurveda, the digestion and metabolism is related to Agni.Mainly the pachaka pitta is responsible for the digestion of food12.The pachaka pitta is situated in Grahani that directly participated inthe digestion of food Grahani is also considered as a pittadharakala. Avastha paka is the first phase and vipaka is the secondphase. Avasthapaka is the first phase of the digestion completed by 7   
  • Pachakagni in Annawaha srotasa, and vipaka is the second phase ofdigestion that completed by Bhutagni and Dhatvagni. vipaka is startafter Avasthapaka.(A) AVASTHAPAKA:-There are three stage of Avasthapaka.(i) Madhur Avasthapaka(ii) Amla Avasthapaka(iii) Katu Avasthapaka(i) Madhura Avasthapaka13:- Four type of Ahara dravyas like Asita, Pitta, Lidha and Khaditathat reaches to Amashaya forms in to Madhura Bhava. At this stagesalivary digestion will be completed in the fundus of stomach, werethe insoluble starch and polysaccharides. Converted in to soluble dextrin under the influence of salivaryamylase. The final Rasa in the upper portion of the urdhavaAmashaya is madhura. The prana vayu is responsible for the entiremovement of food from the mouth to Amashaya. The BodhakaKapha and Kledaka Kapha is also responsible for MadhuraAvasthapaka. Bodhaka kapha is responsible for perception of tastein the mouth. The Bodhaka Kapha is analogue of saliva whichdissolves some substances, the enzyme content begins to act and itlubricates the food, kledaka kapha also lubricates the food inAmashaya. We can considered it as mucine. 14(ii) Amla Avasthapaka :- Amla types of strava occurs here, and after completition of it.Ahara becomes Amla. So it is called Amla Avasthapaka. In thisstage Ahara converting in to insoluble proteins to soluble proteins,under the influence of the pepsin, in the presence of HCL. According 8   
  • to charaka and vagbhatta the final out come of the entire gastricdigestion is the acidified chyme, that is interpreted by Tikakarchakapani as pakvapakva (partialy digested). At this phase theahara pachana is due to an amla factor sereted by the urdhvaAmashaya. The ahara which becomes Amla Bhava, passes in to thenext lower portion of Annavaha srotasa, were Achhapitta issecreted. Modern science says that the acidified chyme passes downfrom the pylorus in to the duodenum. acts as a stimulates theduodeneal glands (Burners gland) to secreate a number of internalsecretion like secretin, cholecystokinin, enterogastrone,Pancreozymine etc. The presence of acid in duodenum is liberatesthe circulation of secretin hormone and stimulate the flow ofpancreatic juice. Secretins also enhance the secretion of bile andintestinal juice. The pancreozymine and intestinal hormone alsostimulates the secretions of enzymes from the pancreas, occurs inintestinal mucosa cholecystokinin also responsible for thecontraction of the gallbladder and therefore discharges of bile induodenum. All these hormeones acts due to entering the acidifiedchyme in to duodemum and there fore pancreatic juices, biles andintestinal juices secreated in small intestine. In Ayuarveda,Achhapitta is combination of these three juices. We can say thatmadern physiology also supports the Ayurvedic approach ofAchhapitta Nirman Kriya. Due to these juices all the Facts and semidigested proteins are completly digested and converted in to fattyacids and glyceral and Amino acids.(iii) Katu Avasthapaka15:- In this stage, the materials phases down the pakvashaya fromthe Amashya and being dried by Agni. and rendered in to lumps.(paripindita pakva) During this process vayu and Mala areproduced. In Modern physiology, minerals from the end products ofdigested food, the remaining materials are converted in to feaces. 9   
  • The bacteria precessed on it and created some vitamins and indoleand sketol like gases.(B) VIPAKA:- According to charaka the digestion of food by jatharagni breakdown the food in to five physicochemical groups viz parthiva, Apya,Agneya, Vayavya and Akashiya. Activated Agni Bhuta present ineach one of these Bhautika groups. The Bhutagni thus activateddigests the substance of that group16.(i) Bhutagni Paka17 :- Bhutagni paka follows jatharagni paka and it completes theprocess of intestinal digestion. After Bhutagni paka, the Ahara Rasais completed and the Rasa shoshana is possible. Thus the Agniconstituents of the predominantly parthiva molecule spoken asparthivagni digest the substances of the molecules. SimilarlyApyagnidi gets the substance of the moleoules of Apya and it forAgneya, Vayavya, and Akashiya, the out come of this type ofdigestion according to chakrapani is the transformation of thecharcteristic qualities of each group and the assumption by them ofvilakshana Gunas or all together new qualities.(ii) Dhatvagni Paka18:- After Jatharagni Paka & Bhutagni Paka of the Ahara Rasa iscreated and it is absorbed from the Anna Vaha Srotasa andcirculates throughout the body by Dhamanies This Annarasaundergoes the process of Dhatvagni Vyapara and thus saptadhatusare created. Seven different kinds of Dhatvagnis correspondence tospecific seven types of Dhatus viz Rasagni, Raktagni, Mansagni,Medogni, Asthyagni, Majjagni and Shukragni. The Rasagni does thedigestion of the Ahararasa so Rasadhatu and its Mala aredeveloped. In the same process every Dhatvagni digests the same 10   
  • molecular particles of Ahararasa and same Dhatus were developed.Acharya Charaka said that the pakas act upon seven Dhatus givingrise to Kitta and prasada bhaga19. The prasada paka is related to anabolic aspects and the kittapaka is of the catabolic. Dhatvagni converts the Ahara rasa in tosthayi & Asthayi Dhatu. Prasada Paka is being an Asthayi Dhatu.Asthayi Dhatu is converted into sthayi Dhatu by particularDhatvagni. In Dhatvagni Vyapara Kitta paka like sveda, Mutra,Purisha, vata pitta, kapha smashru, Nakha, Kesha etc are alsodeveloped. Indian medicine books have given various concepts likekhalekapota Nyaya, Ksheeradadhi Nyaya. Kedari Kulya etc. onDhatvagni Vyapara or Dhatu Nirman.PATHOPHYSIOLOGICAL ASPECTS OF ANNAVAHA SROTASADusti Hetu20(1) Ati matra Bhojana(2) Akalae Bhojana(3) Ahita Bhojana(4) Agni Dusti Meaning of Ati matra bhojana is, the excessive intake of food.Akalae bhojana means irregular patern of food intake. Ahitabhojana means the food taken by the person is not reliable for Phishealth. Agni Dusti means the improper digestive power. First threecausative factors creat Agni Dusti by Dosha Vaishmya. Agni Dustri,the fourth causes is due to some diseases like Rajayakshma. All ofabove causative factors create the disease of Annavaha srotasa likeAmlapitta. They generate the Adadrasha & dusha vaisamya, whichresponsible for the aggravation of the process of the diseases like 11   
  • Ajirna, Chhardi, Atisara, Arasha, Grahani, Amlapitta, Alasaka,Aruchi, Visuchika etc. These causative factors vitiate the pittadharakala. So these symptoms are developed.DUSTI LAKSHANA :-Four main symptoms of the Annavaha srotodusti. They are thecardinal symptoms of the Annavaha sroto dusti.(1) Arochaka (3) Chhardi(2) Avipaka (4) Anannabhilasha(1) Arochaka21:- The loss of taste of food is called Arochaka loss of interestingof food intake even though the food is very good and delicious.Acharya sushruta said that Arochaka is a disease, which hascomplete loss of interest in food due to shoka, Bhaya, Krodha,Lobha etc. Vitiated vatadi doshas and manasika Bhavas that stayingin Jihva, Hridaya and Bhaktayana. According to sushruta, shokadiManasika Bhavas as the causative factors of it. They create vatadiDosha Dusti. vitiated Dosha dusti. vitiated doshas stayed in Jihva,Hridaya and Bhaktayana means the Amashaya and Annanalika so,the Annavaha srotodusti is there.(2) Avipaka :- Avipaka means indigestion of the food. The ahara paka kriyais disturbed due to Agni vaishmya & avipaka is created. The Grahaniis the main organ in Annavaha srotasa as an anatamical andphysiological both. In annavaha srotodusti, Grahani Dosha is there.So, the pittadhara kala and Agni is also distrubed, because there isa reciprocal relationship between Agni & Grahani. In the modern science, the mucosal membrane lined in thestomach and small intestine is responsible for the secretion of 12   
  • enzymes. If there is some distrubance in it, the enzymes are notsecreted in proper way. In this condition the indigestion or Avipakais occurred. Acute & chronic gastritis, peptic ulcer, tropical & nontropicalsprue, malabsorption, syndroimes, non ulcer dyspepsia. etc,disease. have Avipaka as a first symptom In all these diseases innermucous membrance is affected which called pitadhara kala inAyurveda.(3) Chhardi :- Meaning of chhrdi is forceful expulsions of the gastric and / orduodenal contents through the mouth. It is due to Avipaka and AgniVaishamya. Mainly vata Dosha – Udana and Samana Vayudistrubed. It is occured when any part of the upper gastrointestinal tract becomes excessively irrited Impulses are transmittedby both vagal and sympathetic afferent to the bilateral vomittingcenter of the Medulla, which lies near the tractus solitarious. Motorimpulses are tremsmitted though the 5th, 7th, 9th, 10th and 12thcranial nerves to the upper gastro intestinal tract and through thespinal nerves to the diapharm and abdominal muscles. This nervousmechanism is considered as a vitiation of vata dosha in Ayurveda.Mainly observation or anti peristalsis activity is responsible forvomiting. Irritation of mucus membrance like gstritis, enteritis etc isalso responsible for it.(4) Anannabhilasha :- Anannabhilasha means the total loss of desirement or interestof food even though it is given as per demand of the person.Chakarapani has said that the pt. can digest the Ahara in tostomach through the mouth but the loss of interest of food is there. 13   
  • In modern science, it is due to mental stress or sensation of stietywhile complete loss of appetitite is not there. Digestive System 14   
  • CONCEPT OF DIGESTION Gastro intestinal digestion or change in the state or form ofthe food substances in Aamaashaya and Pakvaashaya in the courseof digestive process. Two phases of the Paaka i.e, Prapaaka andVipaaka have been envisaged. The Prapaka has been defined byChakrapanidatta as Prathama Paka22. These changes have beendescribed in terms of the Rasa or taste of the end products ofgastro-intestinal digestion viz. Madhura, Amla and Katu23. Prapakacommences right from the time, when food is introduced into themouth. This aspect of digestion and the digestion in the upperportion of Urdhwa Aamaashaya are comprehended by MadhuraBhava. When the food is introduced into the mouth, the perceptionof its Rasa takes place which is stated to be enabled by BodhakaKapha24. The next event which takes place is Vibhajana of food bythe Tejas element of the Lala Strava, which is described inAyurveda Sootra and Yoganand Natha commentary. Tasteperception and preparatory digestion and the beginning of theMadhura Bhava occurs here. The movements are brought by PranaVayu25. The second phase i.e. Amla Avasthaa Paaka involves theVidagdhavastha of food. The term Vidagdha has been interpreted byChakrapanidatta as Pakva- Aapakvam or Kinchit Pakvam KinchitAapkvam i.e. partly or not fully digested26. As the partly digestedfood which has attained Amla Bhaava is moved down, Achha Pitta issecreted27. The term amla refers to the production of Pitta underinfluence of the Aahaara which has since assumed Amla Bhaava.The third aspect of Avasthaa Paaka is the Katu Bhava. This aspectrelates to the acrid and pungent nature of the reactions that occurin the Pakvaashaya. Charaka says that the material passed downfrom the Aamaashaya having reached the Pakvaashaya isdehydrated and converted into lumps by heat28. 15   
  • Chakrapanidatta has observed that the term Shoshana usedby Charaka instead of Paachana is significant. The former relates tothe dehydration of the food residue which has been brought toPakvaashaya whereas the later refers to the digestion of food in theAamaashaya by Agni. The term Paripindita Pakvasya according tohim refers to the process of formation of fecal lumps. The termVaayu syat KatubhaVaatah describes the production of acrid andpungent gas29. Pakvaashaya is the seat of Vayu where five Vayusare produced. According to Sushruta, the separation of Rasa, Mala andMootra brought about by Paachaka Pitta. Sharangdhara andBhaavamishra have stated that the Saara Bhaaga is known as Rasa,and the Saraheena Bhaaga is Mala. The factors responsible fordigestion is six Ahara Parinama Kara Bhavas30. i.e.i) Ushma ii) Vayu iii) Kledaiv) sneha v) Kala and vi) Samyoga.i) Ushma: Ushma is a quality of Agni mahabhuta only. In thisregard two terms are to be considered i.e. Agni and Pitta. Sushrutaexplains that there is no Agni excepts Pitta in body31. Out of fivetypes of Pitta, Pachaka Pitta situated in Amashaya performs allfavorable and unfavorable functions described as functions of Agnivarious secretion of GIT can be considered in the light of PachakaPitta. So release of these secretions in proper time, quality includingthe temperature of stomach is essential for proper digestion,disturbance of any will lead to Agni Dusti and start the Samprapti ofdisease.ii) Vayu: Samana Vayu is seated in Amashaya and helps thePachaka Pitta in digestion. According to Sushruta31. There is viciousrelationship between Prana - Apana – Samana Vayu. Where as 16   
  • Prana and Apana Vayu helps to maintain the Agni. Prana Vayudirectly takes place in act of digestion by transporting food uptostomach and Samana Vayu moves in koshtha all around andperforms the functions attributed to Agni, Grahani and PachakaPitta. Three phases of gastric acid secretion can be consideredunder the karma of Vayu. That is cephalic phase, gastric phase andintestinal phase. The apakarshana, grahana and munchana karmaof Vayu are essential for proper digestion. Any exacerbate orcessation in these functions will lead to improper digestion. Ascertain time is required for proper digestion, delayed emptying willcause the shuktapaka and formation of annavisha, which are theessential features of Grahani dosha samprapti. Now, it is clear thatall secretory regulations can be said the function of Samana Vayu.Any disturbance of Samana Vayu will cause the Agni Vaishamya,which will lead to Ajeerna etc. and start the pathogenesis. Theetiological factors like Krodha, Shoka, Bhaya, Chinta and otherstress factor work through the vagus chain, which is mediatingthrough Vayu. Provocation of Vata by any factor will result in hypersecretion leading to hyperactivity.iii) Kleda: This factor is necessary for proper digestion. Kleda loosesand emulsifies the food substance. So that it may easily digested33.This function is performed mainly liquid portion of food. Kledaka andBodhaka Kapha may be considered in this regard. Charaka hasmentioned the function of disintegration and softening of foodsubstance in the Koshtha due to ‘Drava’ and ‘Sneha’. Though Kaphahas not been mentioned having Drava quality but Kapha is made upof ‘Ap’ dhatu and so that Kapha most possess Dravata but itdepends upon the temp. so the function of Kledaka Kapha can besummarized as Kledana - Shithilikarana – Mridukarana andSamghata Bheda. Also the functioning of Bodhaka Kapha mayinclude moistening of mouth to help in speech and helps in 17   
  • mastication. Dravata is also the quality of Pitta and Kledana functioncan also be attributed to the dravansha of Pachaka Pitta. Theexcessive klinnata may hamper the Agni directly as mentioned inthe literature that Dravata create the Agni. Ingestion of anyAtiushna, Tikshna and Katu Dravya may cause excessive secretionof mucosa, which may interfare with digestion process and causethe Vidagdha Avastha in excess leading to Ajirna etc. in the sameway increase in Kapha cause Mandhaagni. Hence, if the function ofKapha create, the ulcer can directly be produced due to action ofAgni on mucosa. Hence, a very delicate balance of responsiblefactor is required for proper digestion.iv) Sneha: Sneha mainly comes from Ahara, Kapha also have theproperty of Sneha. Also Chakrapani clarifies that sneha is present infeeble quantities in Pitta. Hence it can be said that sneha is alsoquality of kledaka Kapha and Pachaka Pitta. Sneha performs thefunction of Mardava of food stuff. Ultimately it helps in the propermastication and churning by stomach musculature, so that properdigestion can takes place. The decrease in the quality of Sneha maydamage the intestinal mucosa due to roughness of food stuff andalso due to Ruksha Guna of various food materials. Hence,Snehaguna also performs the protective effect to the stomachmusculature. Decrease of Sneha in stomach will lead to provocationof Vayu (Samana Vayu) which causes imbalance of Agni leading toAgni Vaishamya.v) Kala: Kala means mainly the time required for the digestion ofingested food stuff. Time required for the proper secretion of all thedigestive factors and for proper digestion and absorption. But othertime consideration are also necessary for proper digestion andabsorption of food i.e. Kshudhakala (hunger time). Trishnakala,Doshakala and also Charvana Kala. The meals taken without proper 18   
  • digestion of previous meal is called adhyasana and this untimely,food intake causes Amadosha which leads to Agnidushti. Emptyingof stomach requires certain time, liquid empties rapidly than solid.Timing of relation of food material in intestine is regulated by Vayu.Any disturbance of Vata will disturb the Dharana and Munchanaperiod leading to improper digestion and absorption, which will leadfurther provocation of Doshas and Agni Dushti.vi) Samyoga: Equilibrium of all the above factor is necessary forthe proper digestion of ingested food material. Therefore AshtavidhaAhara Ayatana, 12 Ahara Vidhi Vidhana should be considered sothat Agni Vaishamya and vitiation of Doshas may not take place.vii) Ashtavidha Ahara Vidhi Visheshayatana (eight lines forselection of food)a. Prakriti (Natural Qualities) – before ingestion of food, thenatural properties of food must be considered so that these may nothamper Agni and Doshas.b. Karana (Preparation) – Various cooking procedure may increaseor decrease the properties of food stuffs. This may be due toadmixture of water, heating and predominance of time and season.Also other factors i.e. Desha, Kala and Bhajana (utensils) must beconsidered.c. Samyoga (Combination) – Charaka has discussed 18 types ofincompatible diet. He has also enlisted various diseases producedincluding Amlapitta and Grahani roga due to ingestion ofincompatible diet. 19   
  • d. Rasi (Quantum) – It refers to the total quality of food as wellas quality of various constituents of diet. Every body must eatrequired quality which may directly interfere gastric juice secretionand digestion process. Atimatra and Amatra Bhojana may lead tovitiation of Doshas.e. Desha (Habitat) – This denotes place relating to growth as welldistribution of substance which also direct affect the Agni indigestion process.f. Kala (Time) – Here both Nityaga and Avasthika Kala should beconsidered. Seasonal dietetic variation, age wise variation, day andnight variation and disease wise variation can be considered.g. Upayoga Sanstha (rules of use) – This depends on thedigested food.h. Upayokta – means who consumes the food. i.e. the user. Dietmay vary person to person according to their body compatibility andhabits on him depends the Oka Satmya.Aharavidhi vidhana (code of healthy eating) –Charaka has also prescribed the code of healthy eating afterdescribing the basis for selection of healthy diet which are 12 innumbers. They are –i) Ushnamashniyat – It enhances test, increases Agni, easilydigestible and does Vatanulomana and decrease Kapha.ii) Snigdhamshniyat - It diminishes the Rukshata of ingested foodand regulates the action of Vayu. 20   
  • iii) Matravadashniyat – Quantity is related with individual’sAgnibala. Heena and ati qualities of food create the disturbance inAgni.iv) Jirne ashniyat – Ingestion of food before digestion of previousmeal cause vitiation of Agni and all the Dosha. Hence meal shouldbe taken only after digestion of previous meal.v) Viryaviruddhamshniyat – Intake of Virya Viruddha Dravyas causetridosha prakopa.vi–xi Ekdesha, Ekasarvopakarana, Natidruta Nativilambita TanmanaBhunjita Ajalpannahasanam - All the above factors causes properdigestion of food by which there is no chance of vitiation of Agni.xii) Atmanam Abhisamikshabhunjita – Every user must consider hisself well. Hence all the above factors are responsible for propersecretion of gastric juice and digestion occurs. If any one causevitiation of Pachakapitta/ Samanavayu leads to Agni Dushti.Sushruta has also prescribed the code of behaviour after takingmeal. He has advised walking for at least 100 steps. There aftertaking rest for sitting position for a while and there lying supine inleft side position. This gives proper time for digestion34.According to modern Digestion means the breaking down of larger food moleculesinto smaller molecule. The passage of these smaller molecules intoblood and lymph is termed as absorption. So the organs whichperform both these constitute the digestive system. Digestionincludes 6 basis process i.e. ingestion, secretion, mixing andpropulsion, mechanical and chemical digestion, absorption anddefecation. 21   
  • 1. Ingestion – This process involves taking food and liquid intomouth.2. Secretion – Cells within the walls of GI tract and accessorydigestive organs secret seven liter of water, acid, buffers andenzymes within the tract/day.3. Mixing and Propulsion – Alternating contraction and relaxation ofsmooth muscle in the walls of GI tract mix food properly themtowards anus.4. Digestion – The process of digestion starts from mouth. Twotypes of digestion i.e. mechanical and chemical process break downingested food into small molecules.a. Mechanical digestion – Teeth cut and grind food, then smoothmuscles of stomach and small intestine churne the food. So thatfood molecules become dissolved and mixed thoroughly withdigestive enzymes.b. Chemical digestion – A series of hydrolysis reaction that breakdown large carbohydrates, lipids, proteins and nucleic acid with thehelp of digestive juice (saliva, gastric juice, pancreatic juice, succusentericus and bile) into smaller molecules that are usable by bodycells.c. Mechanical Chemical digestion in mouth Mechanical digestion – Ithelps the process of mastication of the food stuff and in preparing itinto a bolus and suitable for deglutition. Here saliva acts aslubricant. Chemical digestion – two enzymes i.e. salivary amylaseand lingual lipase contribute in it. Salivary amylase initiates thebreak down of starch, into monosaccharides for which it can be 22   
  • easily absorbed into the blood stream. Lingual lipase secreted byglands in the tongue. It breaks down dietary triglycerides into fattyacids and diglycerides.d. Mechanical and chemical digestion in stomach Mechanicaldigestion – It consists of mixing waves (peristaltic movements) bywhich food mix well with secretion of gastric glands and form asouping liquid called chyme and also these waves pushes the chymeinto duodenum through pyloric sphincter. Chemical digestion –Gastric juice secretion from the cells of stomach which takes part indigestion i.e. Cell Secretion Results1. Chief cellsa. pepsinogen Inactivateform becomes activate with the help of HCland breaks down proteins into smaller peptide fragments.b. Gastric lipase Splits short chain triglycerides into fattyacids andmono glycerides.2. Parietal cellsa. HCl - Kills microbes in food.- Denatures proteins in food.- Converts pepsinogen into pepsin.- Stimulates the secretion of hormones that promotes the flow of bile and pancreatic juice.b. Intrinsic factor Needed for absorption of vit. B12, which is used in redblood cell formation. (erythropoiesis)3. Surface mucusa. Mucus forms a protective barrier that prevents digestin ofstomach wall. 23   
  • b. Absorption small quantity of water, ions, some drugs enter theblood stream.4. G cellsa. Gastrin stimulates parietal cells to secrete HCl and chief cells tosecret pepsinogen.- Contract lower oesophageal sphincter,- Increases motility of the stomach and relaxes pyloric sphincter.Regulation of gastric secretion and motility:Both neural and hormonal mechanism control the secretion andcontraction of stomach wall. Gastric digestion occurs in threehases. i.e. -1. Cephalic phase2. Gastric phase3. intestinal phaseCephalic phase: This phase of gastric secretion occurs even beforefood enters the stomach. It results from sight, smell, thought ortaste of food, and greater the appetite, the more intense is thestimulation. Neurogenic signals causing the cephalic phase ofsecretion can originate in the cerebral cortex or in thehypothalamus. They transmit impulses through vagus nerve tostomach. This phase of secretion accounts for one tenth to one fifthof the gastric secretion.Gastric phase: Once food enters the stomach, it excites the gastrinmechanism, which in turn causes a low rate of secretion of gastricjuice that continues throughout the several hours that the foodremains in the stomach. In addition, the presence of food in thestomach also causes- i) local reflexes in the intramural plexus of 24   
  • stomach and ii) vasovagal reflexes that pass all the way to thebrain stem and back to the stomach. Both these reflexes causesparasympathetic stimulation of gastric glands and add to thesecretion caused by gastric mechanism. The gastric phase ofsecretion accounts for more than two thirds of the total gastricsecretion associated with eating a meal.Intestinal phase: Even after the food has left the stomach, smallamount of gastric juice. Continue to be secreted for six to eighthours, i.e. As long as chyme remains into the small intestine.Further more, this secretion will still occur even when all nerveconnections are cut. Further presence of fatty acids and glucose inchyme triggers enter endocrine cells in the small intestinal mucosato release two hormones that affect the stomach ie. Secretin andcholecystokinin. Secretin mainly decreases gastric secretionwhereas CCK mainly inhibits stomach emptying. Also bothhormones have other important effect on pancreas, liver and Gallbladder that contribute to regulation of digestive protcess. Onlyabout 5% of total gastric secretion occurs during the intestinalphase.Pancreatic juice:The enzymes in pancreatic juice digest all the foods i.e.i) Pancreatic amylase – hydrolyzes starch, glycogen and otherCarbohydrate except cellulose.ii) Several protein digesting enzyme i.e. trypsin, chymotrypsin,carboxypeptidase and elastase. Break down proteins into peptides.iii) Ribonucleic and deoxy ribonucleic acid – Both are nucleic aciddigesting enzyme.iv) Pancreatic lipase – hydrolyzing neutral fat into glycerol and fattyacids. 25   
  • The above pancreatic secretion are regulated by nervous andhormonal mechanism.a. Nervous mechanism starts 1-2 minutes after taking food.b. Hormonal mechanism starts when stomach empties intoduodenum. Two hormone i.e. secretin and pancreozymin isresponsible for increased secretion of pancreatic enzymes. Bile –Bile secretion by liver is continuous. Though it contains no digestiveenzyme, but important for digestion because of the presence of bilesalts,which help –1. To emulsify by fat globules so that they can be digested by theintestinal lipase.2. Render the end products of fat digestion soluble so that they canbe absorbed through the GI mucosa into the lymphatics. Machanicaland chemical digestion in the small intestine. Chyme entering thesmall intestine contains partially digested carbohydrates, proteinsand lipids. The completion of digestion is a collective effort ofpancreatic juice, bile, and intestinal juice. Machanical digestion- Itinvolves segmentation and migrating motility complexes.Segmentation mix chyme with the digestive juice and bring theparticles of food into contact with the mucosa for absorption.Migrating motility complex is the type of peristalsis begins in thelower portion of stomach and pushes chyme forward along smallintestine. Altogether, chyme remains in small intestine for 3-5hours.Chemical digestion – various enzymes secretes from the brushborder of the intestine, which also takes part in digestion. Theseare- 26   
  • Carbohydrate digesting enzyme – Brush border enzymes i.e.i) α- dextrinase - acts on α- dextrins to glucose.ii) Maltase - splits maltose, maltotriose into glucose.iii) Lactase - Digest lactose into glucose and galactose.iv) Sucrase - breaks sucrose into glucose and fructose.Protein digesting enzyme –Protein digestion completed by two brush border enzymes. i.e. –i) Amino peptidase – acts on peptides by breaking the peptide bondthat attaches the terminal amino acid to the amino end of thepeptide.ii) Dipeptidase – splits dipeptides into single amino acids.Fat digesting enzyme –i) Lipase (intestinal) – splitting neutral fats into glycerol and fattyacid. Digestion of nucleic acids: The nucleotides result from theaction of pancreatic nucleases are further digested by brush borderenzyme called nucleosidases and phosphatases into pentoses,phosphates, and nitrogenous bases. Mechanical and chemicaldigestion in large intestine-Mechanical digestion – it involves the movements of largeintestine includes haustral churning, peristalsis and mass peristalsisby which the contents of colon drives into rectum.Chemical digestion – it occurs through bacterial action.- It ferment remaining carbohydrates and release hydrogen,carbondioxide and methane gases.- It converts remaining proteins to aminoacids and break down theaminoacids into simpler substances, ie. Indole, skatole, hydrogensulfide, and fatty acids.- It decomposes bilirubine to simpler pigments, including stercobilin, 27   
  • which give faeces their brown colour.- It also produces some vitamins i.e. vit. B and vit. K that areabsorbed in the colon.5. Absorption – The entrance of ingested and secreted fluids, ionsand the small molecules that are products of digestion into epithelialcells lining the lumen of the GI tract is called absorption. Theabsorbed substances pass into blood or lymph and circulate to cellsthroughout the body.6. Defecation – wastes, indigestible substances, bacteria, cells-sloughed from the lining of the GI tract and digested materials thatwere not absorbed leave the body through the anus in a processcalled defecation the eliminated material is termed feces. 28   
  • DISEASE REVIEW The word ‘Disease’ literary means the lack of ease. Accordingto Taber’s encyclopedic medical dictionary, disease means “Apathological condition of the body that presents a group ofsymptoms peculiar to it & that sets the condition apart as anabnormal entity differencing from other normal or pathological bodystates.” Amlapitta is a disease which is commonly found almost allpart of world. Ayurvedic View:HISTORICAL REVIEW: To have a complete knowledge of subject it is necessary totrace out its historical background for the disease Amlapitta one hasto trace out its original concepts various developments at presentstage & the work done on the subject by various research workers.A) VAIDIC KALA : In Vedic literature, showed no suggestive references ofAmlapitta description.B) SAMHITA KALA :1. Charaka Samhita : Acharya charaka has not mentioned Amlapitta as a separateentity but Charaka Samhita has many scattered references ofAmlapitta which are as below.a) Amlapitta has been listed as an indication of eight types of milk35.b) The list of paittika nanatmaj Vyadhi is includes Dhumaka, Amlaka, Vidaha which are the symptoms of Amlapitta36. 29   
  • c) Kulattha has been considered as a chief causative factors of Amlapitta37.d) Excessive use of lavana Rasa has been also considered as causative factor of Amlapitta37.e) Amlapitta has been included in the list of diseases caused by viruddhasana38.f) Rajmasha has the property of relieving the Amlapitta38.g) Mahatikta Ghrita has been indicated in Amlapitta39.h) Amlapitta has been mentiones as an indication of Kansa – Haritaki40.i) In Grahani dosha. Pathogenesis of Amlapitta has been clearly mentioned41. A clear cut samprapti of this disease is available ‘kulatta’,lavan rasa, & viruddhahar were listed as the causes of Amlapittawhere as ‘Mahatikta ghrita & kansaharitaki are prescribed for itstreatment. Hence it can be concluded that during the period ofcharka all aspects of Amlapitta disease were considered.2. Sushruta Samhita Acharya Charaka has mentioned the word Amlapitta but it isnot found in sushruta samhita. Sushruta has mentioned symptom.Known as ‘Amlika’ results from excessive use of Lavan Rasa, issimilar to Amlapitta, ‘Amlika’ word has found in sushruta samhitasu. 21 & 22 & in Nidan sthana – 2 & 6. In the Sanskrit English dictionary by Monier-Monier Williams meaning of Amlika is mentioned as acidity of stomach.3. Kashyapa Samhita Among the ancient texts Kashyap Samhita is the first text,which has mentioned Amlapitta as separate disease. This text has 30   
  • given aetiopathogenesis, clinical features complications &treatment & also gives suggestion to change the place of living tohave good peace of mind to cure the disease thus in the Upanishadkala also it was firmly believed that manasika bhavas are affectingthe disease Amlapitta.4. Harita Samhita Harita Samhita in 24th chapter of 3rd sthana has describedAmlapitta as a separate disease & given the treatment. It alsogives. One special symptoms of the disease as ‘Amla Hikka’(Hiccups with sour taste)5. Bhel Samhita In Bhela Samhita, Amlapitta is not mentioned in this samhita.C) Samgraha Kala1. Ashtang Sangrah & Hridaya Vagbhata I & II were one of the most eminent of ancientphysicians who written the Astanga Samgraha & Astanga Hridyamrespectively. In both these text Amlapitta word & synonyms of Amlapittai.e. ‘Amlak’ is mentioned with scattered references as follows.a) Vagbhata – I also mentioned ‘Dhumaka’ & ‘Amlaka’ in pittaja nanatmaja disorders.b) While describing the symptoms of1. Pittaja Jawara 2. Pittaj Kasa 3. Pittaj Hridroga ‘Amlaka’ is mentioned.c) In the indications of Dashmula-leha “Vagbhata I” mentioned Amlapitta while ‘Vagbhata II’ mentioned ‘Amlaka’. 31   
  • 2. Madhava Nidana After Kashypa Samhita, Madhava Nidana is first available textwhich gives importance to Amlapitta and describes itsaetiopathogenesis & symptomatology in details along with twoclinical subtypes viz.1. Urdhvaga Amlapitta2. Adhoga Amlapitta Vri. Madhav has described Amlapitta is an independentdisease & also its therapy.3. Chakradatta In this classics, vamana, Virechana, Basti etc. treatments areadvised for Amlapitta along with its Chikitsa Sutra thesymptomatology of Amlapitta is given the detailed treatment ofAmlapitta is given by Chakradatta.4. Sharangadhara Samhita Sha. Sa. Being a book of pharmacoped has given onlyAmlapittahara recipes without describing the aetiopathologicalconcepts of the disease.5. Basavarajiyam This text has included the Amlapitta under 24 NanatmajaVyadhi of pitta.6. Bhavaprakasha Two separate chapters on Amlapitta has been devoted in thistext. Upadrava & arista are explained in this text. 32   
  • 7. Yogaratnakara Regarding Amlapitta, he has followed Madhav Nidana totally &this text has added four more upadravas to list of upadravas ofAmlapitta.8. Vangasena Samhita Acharya Vangsena in Vangsena Samhita described Amlapittain 59th chapter as “Amlapitta Rogadhikara”.9. Siddhanta Nidana Detailed information about Amlapitta is given accordingModern medicine. Upadrava one also mentioned.10. Bhaisajya Ratnavali Detailed Chikitsa is given in this Granth same more reliable &more effective Yoga is also describe in this text.11. Rasaratna Samucchaya In this text Amlapitta Nidana Panchaka with its treatment isdescribed in detail. D) Previous Research work On specially Urdhwaga Amlapitta following research scholarshave done work & they were found encouraging results. 1. Tayade V. – Urdhwaga Amlapittapar Patoladi Qwathka Adhyana 1988 – Bombay. 2. Kulkarni A.B. – A study of Avipattikara curna on Urdhwaga Amlapitta 1989-Nasik. 3. Bhande U.M. – Effect of vamana of Katu Nimba & Katu Pravala on Urdhwaga Amlapitta 1991-Pune. 33   
  • 4. Panjihade – Urdhwaga Amlapittaka Samavesat Agnitundi Parinamala Abhysa 1992-Nanded.5. Sephal S.S. – Clinical study of Urdhwaga Amlapitta & effect of Bhunimbadi Rucatha – 1992 – Pune.6. Prasad Kailash – A clinical study of Amalaki kwatha bhavita shankha Bhasma in the Amlapitta 2001- Lucknow.7. Jogad G. – Clinical study on the role of Virechana & Bhunimbadi Vati in the management of Urdwaga Amlapitta – 2004 – Jamanagar.8. Utkalini Nayak – Classification of Amlapitta on Doshik predominance. Their management 2006-Jamnager. 34   
  • AMLAPITTA – AYURVEDIC REVIEW To know the Ayurvedic view about Amlapitta one must gothrough the following factors : 1. Nirukti 2. Paribhasha 3. Paryaya 4. Vargikarana 5. Nidana 6. Samprapti 7. Purvarupa 8. Rupa 9. Upasaya 10. Anupasaya 11. Upadrava & Arista 12. Sadhyasadhyata 13. Sapeksa Nidana 14. Cikitsa Vivechana 15. Pathyapathya Nirukti (Etymology) Amlapitta is a combination of two words : Amla Pitta Sourtaste + Digestivesubstance = Amlapitta Excessive salivation of the human body The terms Amla refers to a particular type of taste equatedwith the sour taste which causes excessive salivary secretion pittais a bodily chemical substance which is mainly responsible for themaintenance of the process of digestion transformation &transmutation on combining both these words the term Amlapittaimplies to a disease or condition in which the sourness of pitta getincreased.Paribhasha/Defination 1. Vachaspatyam According to vachaspatyam, Amlapitta means pitta leading tosour taste. 2. Chakrapani 35   
  • Which means that the quality of pitta i.e. sourness whenincrease leads to Amlapitta. 3. Vijayrakshita Commentator of madhav Nidana defines the words asAmlapitta which means that the pitta having vidahi quality give viseto Amla or sour taste. 4. Shri Gananath sen in his book sidhanta Nidana has givensimilar defintaion of Amlapitta. The above classical description of Amlapitta emphasises thatAmlapitta is a patho-physiological condition in which the pitta getsvitiated in terms of Vridhi (excessiveness) & also the sourness ofpitta is increased.Paryaya/SynonymsPramilaka44 – VagbhatPitta visuchika45 – VagbhtPittamlaka – HaritaAmlika – SushrutaShukta – KashyapaDhumaka46 – VagbhatVargikarana / Classification 1. Madhavkara classified Amlapitta in two ways as follows :a) According to pravriti : Urdhwaga Adhogab) According to Dosha : Vataja Amlapitta Vata kaphaja Amlapitta Kaphaja Amlapitta 36   
  • 2. Kashyapa described this disease in to three types according to Dosha : Vataja Pittaja Kaphaja 3. Yogratnakara & Bhavaprakasa Classified disease according to Dosha as follows : Kapha pittaja Vat-Kaphaja Vataja KaphajaAmlapitta can also be classified according to various factorsas follows – a) Koshthagata – according to its site b) Nija Vyadhi – according to its aetiology c) Amasaya samutpanna vyadhi d) Abhyantara margajaneet vyadhi e) Doshabalapravritta vyadhiNidana / Aetiology After a careful screening & analysis of the etiological factors ofAmlapitta, they may be discussed under four groups. They are a) Aharaj Hetu b) Viharaj Hetu c) Manasika Hetu d) Aagantuja Hetu A brief resume of these factors may be presented as under47Aharaj Hetu (Dietary factors) The first & the foremost group of etiological factors ofAmlapitta may be considered as the dietary factors. Under thisgroup the intake of food against the code of dietetics i.e. AharaVidhi Vidhana & Ahara Vidhi Visheshaayatana is included. 37   
  • Various type of incompatible substance excess of pittaaggravating factors like katu Amla, Vidahi etc. & irregular time ofconsumption of food are the factors against the dietetic code & theyare directly responsible for the annoyance of pitta. a) Viharaj Hetu (Habit oriented factors) To maintain the sound & good health one has to follow thecode of habits. He is required to have regular habits of defecationeating & sleeping in time. He has not to suppress the natural calls.Maintain the equilibrium of the body constituents and by that,obviously, he would maintain good health & proper functioning ofthe body. If this is not followed regularly, the whole functioning ofthe body will be disturbed & in long run; they will cause thedisturbances of the equilibrium of pitta & digestion which ultimatelywill lead to Amlapitta. b) Manasika Hetu (Psychological factors) Psychology also plays a great role in maintaining the health of aperson. An abnormal psychology of a person in terms of anxiety,anger, greediness, etc. would affect the physiology of the digestion.These factors tend to affect the secretion of the gastric juice & bythat, they are disturbing the homeostasis which interns Amlapitta. c) Agantuja Hetu (Other related factors) Now a days Gastrogenic diseases are common. Amlapitta couldbe a sequel of faulty drug use. Over the counter intake of nonsteroidal anti-inflammatory drugs & antico-agulant cure one diseasebut it can produce Amlapitta, Ayurvedic drugs specially unpurified &faulty Rasa Aushadhi may cause Amlapitta. Even Ushna, Tikshnadrug if used excessively without proper assessment of disease for along period may produce Amlapitta similarly panchakarmas withHeenayoga or mithya yoga or Atiyoga lead towards many diseases 38   
  • by attacking on Agni hence Amlapitta also can be seen as anUpadrava of some other diseases like chronic Vibandha, Arsha,Ajirna, Pandu.1) Ahara group48a) According to the type of Ahara Kulattha Pruthuka Pulaka (Husky food)b) According to the quality of food Abhisyandi Gurubhojya Atisnigdha Vidhahi Anna Ati ruksha Vidahi panac) According to the Samskara of the Ahara Apakwanna sevana Bhristadhanya sevana Isksuvikara sevana Pistanna sevanad) According to Dusitanna Dusta anna sevana Paryusita anna sevanae) According to the pitta provocative potency of diet. Adhyasana Ajirnsana Ati drava Ati Usna Ati Amla Ati Tikshna Virruddhasanaf) According to the capacity of weakening the digestive power Ati snigdha sevana Ati Ruksha sevanag) Faulty dietary habits Akala bhojana Antarodakapana Kala anasana Visamasana 39   
  • h) Miscellaneous Annahina madya Madya sevana Gorasa sevana2. Vihara Group49a) Atisnatb) Ati avagahanatc) Bhuktwa bhuktwa diwasvapnatd) Veganam Dharaname) Shaiya prajagaran3. Manasa Group50a) Chinta b) Shoka c) Bhaya d) Krodha e) Moha4. Others –Other factors are –Ayurvedic drugs especially unpurified and faulty Rasa Aushadhis.Ushna and Tikshna drugs if used excessively without properassessment for a long period. Panchakarma with heenayoga,mithyayoga and atiyoga by attacking on the seat of Agni i.e.Amashaya. Upadrava of some diseases like chronic vibandha, Arsha,Ajirna and Pandu. In ayurvedic texts it is noted that sight and smellof certain food items provoke a strong reflex vomiting in whichstomach is powerfully irritated. Also Desha, Kala, Ritu takes a greatextent in the causation of Amlapitta i.e. –Deshaprabhava: According to Acharya Kashyap the disease ismore predominant in anupa desha comparing to other deshabecause of Kapha provocating nature51. In the line of treatment hegives its importance to change the place in untreated cases52. 40   
  • Kalaprabhava: Amlapitta is a chirakalina vyadhi this kala or timefactor is responsible for physiological/ anatomical structure of thebody i.e. Balavastha, Madhya and Vriddha Vastha. The disease ismore prevalent in middle age due to Pittapradhanya. Also paittikadisorders are more prevalent during Pitta provocation time that isduring mid-day and mid-night.Ritu prabhava: This group includes disease which is caused by themeteorological changes such as variations in atmospherictemperature, hot or cold, humidity or dryness, rain and winter,incidental to changes in the seasons. The rainy season isresponsible for amlavipaka of water (due to weakened digestionpower and vitiation of Vata and other Doshas) and eatables, whichin turn vitiates Pitta and Kapha.Modern view –According to modern the aetiological factors (of P U and gastritis)may be as follows –i) Genetic factors:Involvement of blood group O & A and presence of ulcer history infamilies prove relation of genetic factors. Probably the blood groupmodifies the oxyntic cell population.ii) Dietary factors:Irritant food materials such as rich and spicy diet, hot tea andcoffee, pickles etc. are responsible for stimulation of gastricsecretion.iii) Trauma:Due to passage of any solid matter, pyloric obstruction or stenosisresulting, from cicatrical changes following the ulcers, Chronic 41   
  • Functional spasm, carcinomia and congenital defects are alwaysassociated with gastritis.iv) Drugs:Coricosteroids, xanthine, aspirine, alkaloids, NSAIDS, reserpine arereported to be the predisposing factor.v) Neurogenic and psychosomatic factors:There is a well recognized association between mental stress andhyperchlorhydria.vi) Nicotine and alcohol:Alcohol directly damages the gastric mucosa and produces ulcer.Smoking has been reported to produce the amount of prostaglandinE2 in gastric juice and to inhibit prostaglandin synthesis in gastricmucosa.vii) Predisposing factors:Duodenal ulcer occurs specially in energetic ambitious young menwho have irregular and often hurried meals and tend to over work.Such as in Bus drivers, business executives, medical practitionersetc.viii) Endocrine factors:Emotional and systemic stress can act on the stomach throughhormonal as well as nervous pathway, namely hypothalamus, ant.Pituitary, ACTH, adrenals, cortisone and gastric glands. (Sincepeptic ulcer is more common in males it has been suggested thatestrogen hormones may protect against the development of ulcers.Moreover, specific endocrine disease or condition have been provedto be associated with peptic ulcer i.e., excessive adrenocortecal 42   
  • activity, hyperparathyroidism. Zollinger Ellison syndrome multipleadenoma syndromes.ix) Social factor:It is reported that a markedly increased incidence of gastritis foundin unhygienic and lower social economical classes.x) Reflexes: Reflex stimuli from heart, pleura and other organs in the bodymay also set up gastric symptoms. Patients having bronchiectasis orPTB also shows symptoms of gastritis and gastric ulcers. Stressulcer i.e. Curling and Cushing ulcer are included under peptic ulcer.In Curling ulcer excessive burn of skin cause more secretion ofadrenaline and noradrenaline which mixed with circulation andstimulate HCl Producing gastroduodenal ulcer. Whereas in Cushingulcer raised intracranial pressure due to head injury causesstimulation of parasympathetic responsible for increased secretionof HCl lead to peptic ulcer.Infection: Helicobactor pylori plays a significant role in developinggastritis also a number of viral, fungal and other bacterial infectionwere accompany by gastritis.Samprapti:According to Ayurvedic concept, for the proper manifestation of aDisease the vitiated Doshas and dushyas unite in several stages.These stages are known are Kriyakalas, which mean, it guides theproper time for treatment at a particular stage of Doshika imbalancein a given disease. Various stages is very necessary for earlydiagnosis as well as for prompt treatment and for adoptingprophylactic measures at the onset. Therefore, in explaining the 43   
  • samprapti, it is very appropriate and logical to take the Sushruta’sconcept of kriyakala with six clear cut stages. They are-1. Sanchaya (accumulation of Doshas)2. Prakopa (excitation)3. Prasara (spread)4. Sthana Samsraya (localisation)5. Vyakti (manifestation)6. Bheda (final stage of complication) One can call a group of signs and symptoms as a disease,only when the Doshas and dushyas undergo upto vyakti stage in aparticular and a special pattern which is called the melaka visheshaor end product of Dosha dushya samurchhana. Similarly in themanifestation of all diseases, Dosha, dushya and malas are thecommon factors also some other factors are responsible i.e.Rogamarga, Adhisthana, Sanchara, Udbhava, Agnimandya, Amaand Strotas. Samprapti ghataka is necessary before starting todiscuss samprapti.Samprapti Ghataka of Amlapitta The different components producing Amlapitta are as follows :  Udabhava – Amashaya & Pittadharakala  Sanchaya – From pittadharakala to Shleshmadharakala of Amashaya and Pachyamanashaya  Adhisthana – Adhoamashaya  Strotas – Annavaha, Rasavaha, Purishvaha, Raktavaha.  Dosha – Pachaka pitta, Samana Vayu Kledaka Kapha  Dushya – Ahara Rasa, Rakta  Agni – Jatharagnimandhaya  Ama – Jatharagnimandhaya janya ama  Swabhava – Chirkari 44   
  •  Vyadhi – Amashayotha  Rogamarga – Abhayantara rogamarga  Paradhanta – Pitta dosha pradhanya  Prabhava – DarunaDosha- In pathophysiology the involved sites of lesion anddisturbance are Pachaka Pitta, Samana Vayu and Kledaka Kapha.Samana vayu – It controls all the secreting and motility functionsof the two Ashayas and helps in the action of digestive enzymes,assimilation of end products of food and their separation intovarious tissue elements and when vitiated, it causes indigestion,diarrhoea and defective assimilation.Pachaka Pitta- The Amlaguna and Dravaguna of Pachakapitta getvitiated. Kledaka Kapha situated in amashaya is to counteract thedestructive action of Pachaka Pitta. Due to imbalance of Pitta thePachana Kriya is also disturbed. This leads to the formation ofVidagdhajeerna then to Suktapaka and later to Ama.a. The term ‘Ama’ means Apakva Annarasa. If Anna is not properlydigested then the out come of such an Apakva Rasa is Ama.b. Due to impairment of Kayagni. The Annarasa is not properly formand in this state, it is known as Ama.c. The undigested Annarasa possessing foul odour and excessivestickness deprive the body of its nutrition causes sadana. This stickysubstance is known as Ama. 45   
  • e. Due to poor strength of jatharAgni residue of ahara rasa is stillleft behind undigested towards the end of digestion. It is ama whichis root cause of all diseases.f. The first stage or phase of Dosha dushti s also known as ama.When this ama is combined or impregnated with tridosha orsaptadhatus or with malas. Then they are called Sama. The diseaseproduced is also called as Sama rogas.Symptoms of Sama Doshas –Samavata Samapitta SamaKaphaVibandha Durgandhi AvilaStambha Haritam Shyavam TantulaAntrakunjaam Amlam StyanaVedana Ghanam PralepiShopha Guru PichhilaNistoda Amlikarkaram KandhdesheAdhmanam Kantha-Hrid AvatishthateAsanchara Dahakaram Kshudrudgaravigh atakaraAgni – Sushruta explains that the prana, samana and apana whileremaining at their original sites maintain Agni54. The vitiation of anyone of these may lead to Agni dushti and sometimes vitiation ofAgni may lead to disturbance in function of these three or any oneof them. Amashaya and grahani are the place of Jatharagni i.e.Pachakapitta55. The function of Agni performed with the help of samana vayu(for proper digestion). Kledaka Kapha and partially Bodhaka kapha,(protects host body from damage). Any type of disturbance of Agnimay start the pathogenesis i.e. Vishamagni, ii) Tikshnagni and iii)Mandagni, which are said to be the work of tridosha. As the disease 46   
  • of GIT are caused due to Agni Dushti, hence, all the three doshasmay affect the Agni but the manifestation may be according to thedominance of three Doshas. Kashyap Samhita is the first whichexplains the symptoms of Amlapitta according to involvement ofpredominat Doshas.Srotas – The disease involve Amashaya, Grahani and Pakvashaya.Hence Anna and Purishavaha Srotas seems to be mainly concernedbut the Rasavaha Srota which receives the first Ama Visha produceddue to Agni Dushti may get involved. Regarding the types ofSrotodushti the three types of disturbance of Annavaha andPurishavaha can be observed i) Sanga, ii) Atipravritti and iii)Vimarga Gamana.Dushya – While reviewing the symptomatology of Amlapitta andGrahani, it seems that the main Dushya may be Rasa. This is thefirst dhatu to receive the Ama Anna Rasa. The aetiological factorsand symptomatology is also suggestive of Rakta Dushti.Mala – “Na Vegan Dharyet”Ayurved gives one of the most important cause of diseasesaccording to Ayurvedic conceptualization is Vegavarodha i.e.suppression of natural urges.eg. Micturation, defaecation, hunger and sleep, etc. This supressionof natural urges affects the sphincteric competence adversely.Natural contractility and motility of smooth muscles of variousviscera, the GI tract and the macro and micro channels of the bodyare also affected adversely. Once the sphincter of various srotas orchannels get affected, it leads to abnormality in them leading toaccumulation and later vitiation of Doshas. 47   
  • Samprapti of AmlapittaIn vrihatrayee, the disease has not been mentioned in detail but inCharaka samhita the Amlapitta terminology is used at variousplaces. Though Charaka has not mentioned it as a separate diseaseentity, but in the context of grahani chikitsa he has explained theetiopathogenesis of disease. The etiological factors like Abhojana,Atibhojana, Veganigraha, Panchakarma Vyapat and seasonalvariation etc. cause vitiation of Doshas and Agni which ultimatelyresults Mandagni which is treated as mother of all the diseases. ThisMandagni leads to Avipaka and due to Avipaka even light and smallmeals are not digested. This undigested and ill digested food getsshuktatva which leads to the formation of Annavisha. ThisAnnavisha is manifestated in the form of Ajirna56. Nidana sevana Agni dushti Dosha dushti Ajirna Shuktatva Annavisha Amadosha As per Charaka it is said that when diet is not properlydigested it gets formented and forms Annavisha. This Ama whenmixed with Pitta then it develops the disease Amlapitta. UsuallyDravaguna and Amlaguna of Pitta vitiates causing Vidagdhajirna atthe initial stage. If neglected as suggested in Siddhanta Nidana57.This will progress causing inflammation and erosion ofsleshmadhara kala of amashaya leading to manifestation of GrahaniRoga. 48   
  • Kriyakala –Sanchaya – Stage of Agni dushti may be described as the stage ofsanchaya i.e. Due to Sanchaya of Pachaka Pitta, Samana Vayu andKledaka Kapha at their own place i.e. Amashaya.Prakopa – This stage may include the stages of Vidagdha Anna,Shuktapaka of Annapana and Visharupata leading to Ajirna. Thesymptom of this stage may be according to main Dosha involved.Prasara – This stage may differentiates ajirna like – Amajirna,Vidagdhajirna and Vishatabdhajirna due to involvement of doshaswith Visharupa Annapana. Also it is noted Manovaha srotas getsvitiated due to excessive manifestation of various mental factorscausing symptoms of Ajirna and Amlapitta.Sthana sanshraya – This is the further stage and from here thespecific pathogenesis of each disease starts according to thespecificity of Nidanas, quality of Doshas by which they are vitiatedand the place of khavaigunya. So, the three Doshas Samanavayu,Pachaka Pitta and Kledaka Kapha may get Sthana Sanshrita inAmashaya (including Grahani) where simultaneously khavaigunyamight have been produced by the same nidanas or by any othernidana. The symptoms produced in this stage may be same assymptomatology of the Amlapitta and having less severity. Iftratement is not done in this stage the pathogenesis may proceedfurther and may produce the disease like Parinama Shula. This isthe stage from where the Vidagdhajirna can be separated fromAmlapitta. Vidagdhajirna is an acute stage occurring due to nidanasdirectly. And is Nidana Sapeksha, which means after theMithyaahara Vihara of Pittaprakopa diet articles will lead tovidagdhajirna, but here the Doshas have not established theiraffinity with any organ on tissue and only langhana or time will cure 49   
  • the condition, but symptoms may be produced again and againwhenever the Mithyaahara and vihara will be done. But due to againand again provocation, the Doshas will establish their affinity inAmashaya and Grahani (sthanasamshraya). After this stage eventhe laghu and Alpa Bhojana will cause shuktatva and Vidagdhata toAnnapana leading to the production of Amlapitta Roga.Vyakti – At this stage the symptoms of disease Amlapitta may getwell established and further differentiation in Doshik varietiesaccording to predominance may be established. The three Doshikpredominant subtypes of Amlapitta have been advocated byAcharyas i.e. Vatika, Kaphaja and Vatakaphaja. Madhavakara hasalso given a separate classification according to the expulsion rootof Doshas i.e. Urdhvaga and Adhoga types.Samprapti of Amlapitta (interms of Charaka)1. Sankhya sampraptia. Two types according to Gati.i. Urdhvagaii. Adhogab. Three types according to Kashyapi. Vatolvanaii. Pittolvanaiii. Kapholvanac. Three types according to Madhavakarai. Vatikaii. Vata kaphaiii. Kaphaiv. Also counted fourth types as shleshma Pitta 50   
  • 2. Vidhi Samprapti –a. i. Nija ii. Agantukab. i. Svatantra ii. Paratantrac. According to curability –i. Naveena - curable by tactful persuationii. Chirothita - krichhra sadhyaiii. Chirothita – yapya3. Vikalpa samprapti –i. Vata - Chala, Ruksha, Karmatahii. Pitta - Dravyatah, Ushma, Tikshna, Sara, Amla, Katu, Dravaiii. Kapha - Dravyatah, Karmatah, Guru, Mridu.4. Pradhanya samprapti –i. Pitta - Vriddhatamaii. Kapha - Vriddhataraiii. Vata – Vriddha5. Bala – kala visheshaa. Seasonal aggravation i. Sharada ii. Greeshmab. Day/ night i. Noon ii. Mid-nightc. Dietetic time i. BhojanottaraBheda – When the disease progresses further it reaches to sixthstage. Due to the manifestation of various symptoms, the diseasecan be categorised as Vatika, Vata Shleshmika or Shleshmapitta asdescribed by Madhavakara. Due to further involvement of Vata andRakta, the disease can produce Parinama Shula, as a Upadravas oras Nidanarthakaratva. 51   
  • SHADAVIDHA KRIYAKALA OF AMLAPITTA Kriyakala Name TreatmentUse of Ahara withoutfollowing the AshtavidhaAhara Ayatana and AsanaPravichara Agnidushti I Sanchaya NidanaParivarjana Ajirjna II Prakopa LanghanaFurther Dosha prakopa due to their own Nidana III Prasara Special protection Amlapitta Raktagata Vyamalata Grahani Shotha IV Sthanasansraya Early detection prompt treatment Grahanivrana Kaphapittavrita Vata V Vyakti Limitation of disabilityDoshik type of manifestation Upadravagamana Amashayagata Rakta VI Bheda Rehabilitation Pakvashayagata Rakta Bhinna KoshtaFurther manifestation of symptoms of Amlapitta Doshik variance Upadrava Rupata 52   
  • Swatantra and paratantra status of Amlapitta – The above pathogenesis described for production of Amlapittashows that this is a Paratantra Vyadhi produced by one another. But Swatantra type occurs, due to the potency andmultiplicity of Nidanas, diminution of Vyadhi, ofUtpadapratibandhaka Shakti and due to such other reasons,Amlapitta may be caused directly. Hence if the nidanas are sostrong it causes vitiation of Doshas and Dushya, producing Shothain Pitta Dhara Kala of amashaya and grahani lead to occurance ofAmlapitta roga.Different opinions regarding samprapti of Amlapitta- Acharya Kashyap was the first to analyze the disease onDoshik basis, he described the samprapti in detailed. He believedthat (the disease caused by vitiation of three Doshas (Vatadayah)causing Mandagni leads to Vidagdhajirna manifesting as Amlapitta.Whereas Madhavakara describes the development of Amlapitta dueto vitiation of pitta which is already increased due to its own cause.Also Kashyap considered Apakva Madya and Dugdha as causativefactor, whereas Charaka lists Dugdha as one of the pathya forAmlapitta. Harita counts Guda as the causative factor for Amlapitta.In the management, single drugs like Haritaki, Pippali and Rasonawere advised by Kashyap whereas Kapittha, dadima and dhatriadvised by other of Yogaratnakara among the comound drugs‘Narikela Lavana” suggested by author of Rasatarangini, NarikelaKhanda, soubhagyasunthi, Shunthi Khand suggested by BhaisajyaRatnavali etc.are the good remedies for Amlapitta. On analyzing,the pharmacodynamics of these above drugs proved effective in themanagement are contraindicated in increased Pitta condition. 53   
  • Where as the drug of choice should be tikta and madhura rasapradhana. Even present day scholars have ventured on research oneffect of drug like Amalai, Shatavari, Madhuyukta, Guduchi,Bhringaraj, Patol, Pippali, Puga, Udumber etc. in the managementof Amlapitta. That’s why Doshik predominance has been consideredand stressed on the classification according to Kashyap and even byMadhavakara.Why pitta kapha classification considered not Vata?a. Acharyas decribed that diseases are not produced due to anysingle Dosha but by all the three Doshas58. Also they explained thatnon-compliance of healthy eating causes the vitiation of threeDoshas simultaneously. So, whenever Annavisha mixed withSamsrijyamana Pitta (Pitta predominant Tridosha). It will causesPaitika disorders. In the same way whenever Annavisha mixed withVatasamshrista and kapha Samshrista (Vata predominant andkapha predominant tridosha).It leads to Vataja and Kaphaja disorders respectively. So, all thedisease produced are Tridoshajanya.b. Madhavakara explained that Pitta is responsible for thepathogenesis of Amlapitta, but the Nidana like Viruddha Ahara hasbeen enlisted which is said to be the causative factor of threeDoshas.c. Samanavayu, Pachaka Pitta and Kledaka Kapha may get SthanaSanshrita in Amashaya. And these have various relation ship. Whenvitiation of any one, may disturb the others. Kledaka Kapha protectsthe amashaya by counteract the secretion of Pachakapitta. AlsoSamana Vayu maintains / balances the Agni and proper digestion.So when Vata gets vitiated, it seems the possibilities due to 54   
  • margaavarana from Pitta and Kapha. Hence Amlapitta is a diseasecondition produced due to Pitta Kphavrita Vata.d. Kanthadutta has classified that like Kotha, the causative factorsof Amlapitta are kapha and pitta. He has further clarified thatthough the pitta is chief Dosha in Amlapitta, Gaurava, Udgara andKampa symptoms are due to Kapha and Vata respectively. Hence itis clear that Kapha pitta Doshas are the main involved in the patho-physiology of disease.e. Chakrapani explains that urdhva amashaya is the seat for Kaphaand adho Amashaya is the seat for Pitta. Hence Kapha and piitapredominace should be considered due to the predominace. There ismore chances of involvement of local factors in pathogenesisprocess.f. Acharya Kashyap quoted the Doshas as ‘Vatadayah’ but later hehas stressed that the dominant Doshas are Pitta and Kapha59.SAMPRAPTI The word samprapti is the process of disease formationbeginning right from the contact of the causative factor with thebody to complete manifestation of the symptoms. It is a coursefollowed by a disease in which a Dosha get vitiated & the path itfollows for the manifestation of disease. The same idea is reflectedby the word pathogenesis used in the modern medicinal sciences. Kashyap, Madhava & Gananatha sen have mentioned specificSamprapti of Amlapitta as follows. Over indulgence in above mentioned factors cause vitiation ofvata & pitta doshas Anyone of the involved doshas slackens 55   
  • jatharagni (to below normal level) i.e. jatharagnimandhaya. Duringthe stage, what so ever food is consumed becomes vidhagadha.Then it becomes Shukta & it lies in the stomach stagnant. Any food,which is taken, becomes Vidhaga, at this stage Vidhagadhajirnamanifests which is the purvarupa of the disease Amlapitta. Further vitiated pitta get mixed with shukta & causes pittaAma Visha samurchhana. The disease Amlapitta with its cardinalsymptoms is then takes place. If not treated properly in this stage the disease leads toBheda avastha where the typical Characteristics & types likeUrdhavagata & adhogata are differentiated. Further, complication like shita pitta, Udarda, Kotha, etc. aredifferentiated. 56   
  • The samprapti of Amlapitta can be shown into schematic diagram as below : Nidana sewana Aharaja Viharja Manasika Agantuja Pittadhika tridosha prakopa Increase the gastric secreation & or damage the gastric mucosa Pachaka Pittadika Kledaka Kaphadhikya Amasaya dusti Amla gunadhikya Dravagunadhikya pittapradhana of pitta of pitta tridosha prakopaVidagdhavastha of pitta Overcome the Usnagana of pitta Agni dusti Agnimandya Punacha nidana sewana Vidagdhavastha of Anna Shuktpaka Amotpatti Rasadhatu dusti Raktadhatu dusti Annavaha srotodusti Purisavaha srotodusti Atipravritti Vimargagamna Amlapitta Urdhag Adhoga 57   
  • Purvarupa In Ayurvedic classics, no specific purvarupas of Amlapitta arementioned but by applying tarka & pratical knowledge someimportant inferences can be drown. As already explained in the sampropti Agnimandya & Ajirnaare the successive stages towards the manifestation of Amlapitta.Also they are practically observed in the patients. Annavaha &purishavahasrotodusti symptoms can also be considered aspurvarupa of Amlapitta. RupaRupas or Lakshanas are useful for the clinical knowledge of adisease symptomatology of Amlapitta has been described byKashyap, Madhavakara and Harita. Later workers of Sangraha kalaviz, Bhavamishra, Vangasena, and Yogaratnakar have blindlyfollowed Madhavakara in this regard Basavarajiyam has includedAmlapitta in the Nanatmaja diseases of Pitta and given three newsymptoms i.e. Swarahinata, Vak-jihva Paridosha. The generalsymptoms ofAmlapitta described by madhavakara as follows53.- Avipaka - Tikta-Amla Udgara- Gaurava - Klama- Utklesha - Hritdaha- Aruchi - KanthadahaKashyap added extra symptoms like –AntrakujanaUdaraadhmanaVidbhedaHritshula etc. 58   
  • On analysing the classical references pertaining to Amlapitta,it is revealed that quite a big list of symptoms may be prepared.Below a comparative table of the symptoms of Amlapitta is beingpresented on different authorities.Symptoms K.S. H.S. M.N. B.P. Y.R. S.N.Avipaka - - + + + -Amlautklesha + - - - - -Amlaudgara - - + + + +Amlahikka - + - - - -Angasada + - - - - -Antrakujana + - - - - -Aruchi - - + + + -Bhranti - - - - - +Dahayuktatisara - - - - - +Gaurava - - + + + -Gurukosthata + - - - - -Hritshula + - - - - -Hritdaha - - + + + +Kanthavidaha + - + + + +Klama - - + + + +Romharsha + - - - - -Shiroruja + - - - - +Tiktodgara - - + + + -Tiktasya - - - - - +Udara Adhman + - - - - -Utklesha - - + + + -Uro Vidaha - - - - - +Vanti + - - - - - 59   
  • Symptoms of Ekadoshaja AmlapittaSymptoms K.S. H.S. M.N. B.P. Y.R. S.N.VatikaAngasada + - - - - -Jrimbha + - - - - -Shula + - - - - -Snigdha Upasaya + - - - - -PaittikaBhrama + - - - - -Sitaupasaya + - - - - -Svadupasaya + - - - - -Vidaha + - - - - -SleshmikaChhardi + - - - - -Guruta + - - - - -Ruksha Upasaya + - - - - -Usma Upasaya + - - - - -Vatadhikya AmlapittaBhrama - - + + + +Cimcimatva - - + + + +Gatra Sada - - + + + +Harsha - - + + + +Kampa - - + + + +Murccha - - + + + +Moha - - + + + +Pralapa - - + + + +Shula - - + + + +Tamodarshana - - + + + +Kphadhikya AmlapittaAruchi - - + + + +Agnimandya - - - - - + 60   
  • Gaurava - - + + + +Jadyata - - + + + +Kandu - - - - - +Kaphanisthivana - - + + + +Lepa - - + + + +Nidra - - - - - -Sada - - + + + +Sheeta - - + + + +Vami - - + + + +Pitta – Sleshma AmlapittaAmlodgara - - + + + -Aruchi - - + + + -Alasya - - + + + -Bhrama - - + + + -Chhardi - - + + + -Hritdaha - - + + + -Kanthadaha - - + + + -Kukshidaha - - + + + -Murchha - - + + + -Mukha Madhurya - - + + + -Praseka - - + + + -Shiroroga - - + + + -Tikta-udgara - - + + + -Vishishta Lakshana of Urdhvag AmlapittaSymptoms K.S. H.S. M.N. B.P. Y.R.Abhuktevami - - + + +Abhukte va tiktavami - - + + +Abhuktetiktaudgara - - + + +Abhukteamlavami - - + + + 61   
  • Bhukte vidragdhatiktavami - - + + +Bhukte vidhagdha Amlavami - - + + +Bhute vidagdha Tiktodgara - - + + +Caranadaha - - + + +Hritdaha - - + + +Karadaha - - + + +Kukshidaha - - + + +Kandu - - + + +Kanthadaha - - + + +Mandal - - + + +Mahati aruchi - - + + +Pidika - - + + +Shiroruja - - + + +Usnata - - + + +Vanta harita - - + + +Vanta pitta - - + + +Vanta neela - - + + +Vanta Krishna - - + + +Vanta arakta - - + + +Vanta raktabha - - + + +Vanta ativamla - - + + +Vanta mamsdokabham - - + + +Vanta atipichilla - - + + +Vanta Atiachha - - + + +Vanta Sleshma anujata - - + + + 62   
  • Adhoga AmlapittaSymptoms K.S. H.S. M.N. B.P. Y.R.Analasada - + + + -Anga pitata - + + + -Bhrama - + + + -Daha - + + + -Harsha - + + + -Hrillasa - + + + -Murchha - + + + -Moha - + + + -Vividhapradosa - + + + -Adhoyan - + + + -Trita - + + + -Sweda - + + + -Kotha - + + + - 63   
  • Upashaya – Anupashaya:These factors provide a diagnostic aid for the disease which areotherwise difficult to diagnose. Specific description about upashayaand anupashaya is given only by Kashyap while describing Doshajatypes of Amlapitta.Vataja Aamlapita – Snigdha UpashayaPittaja Amlapitta - Swadu and Shita UpashayaKaphaja Amlapitta - Ruksha and Ushna Upashaya Upadrava – Complications of Amlapitta have not been described byancient Acharyas except Kashyap. He has mentioned Upadravas andstated that the disease is incurable in their presence. Also AcharyaGananath Sen has given Upadrava of Amlapitta. These are –SYMPTOMS K.S. S.N. SYMPTOMS K.S. S.N.Jwara + - Shitapitta - +Atisara + - Udarda - +Pandu + - Kandu - +Shula + - Mandala - +Shotha + - Vicharchika - +Aruchi + - Vishphotaka - +Bhrama + - Pidika - +Grahani kshata - + Asamashaya kshata - + Though madhavakara has not mentioned the complication ofAmlapitta, but included shoola in its vatika predominant variety.Hence, Parinama and Annadrava Shula can be taken ascomplication of Amlapitta. 65   
  • Shadhya asadhyata – Madhavakara has pointed out that, if the disease is of recentorigin. It can be cured with proper efforts. In chronic conditionrecurrence occurs where treatment is stopped. In some patients itbecomes more difficult to cure even with proper treatment, so thedisease becomes sukhasadhya when it is of short duration, Yapyawhen it is chronic and kruchhrasadhya when the duration of diseaseis long and cured with great difficulty60. Kashyap has indicated thatif it is accompanied with other Upadravas and Dhatu Kshinata thenit becomes Asadhya61. Chikitsa Ayurveda has emphasised 3 basics of chikitsa regarding alltypes of diseases.i. Nidana Parivarjana - It is to be advised the patient to avoidsuch aggravating factors of ahara and vihara which are responsiblefor causation of the disease. So only wholesome and beneficialdietetic articles are to be provided along with compliance AharavidhiVisesayatana..ii. Apakarshana – Apakarshana mean pacification of Doshas eitherby Shodhana or Shamana or by both. So far Amlapitta is concerned,it is originated in Amashaya and mostly the Doshas are localizedthere. For this condition Vamana is the best treatment. If Doshasare localized in Pachyamanashaya, then Virechana is the idealtherapy. In Shodhana therapy Vamana is advocated in UrdhagaAmlapitta and Virechana in case of Adhoga Amlapitta use ofNiruhabasti is stated by Chakrapani, Vrinda Madhava and GovindDas. Whereas Vangasen and Yogaratnakar has mentioned the useof Raktamokshana. 66   
  • iii. Prakritivighata – It means use of drugs resuscitation ofDhatus. Such treatment is termed as shamana therapy. Hencedrugs having Pitta/ Kapha shamaka property according topredominant Doshas have been prescribed but these drugs shouldbe good for Rasa, Rakta and Annavaha Srotas. Prakruti vighata means the sanshaman chikitsa the root of thedisease must be ruled out for curation and it can be possible withthe help of prakrutivighta. Without sanshodhan karma, onlysanshaman may help for removing the vitiated Doshas. The drugthat removes the vititation of theDoshas and not expulses it fromthe body is called as sanshman karma62 shansaman chikitsa bringsthe imbalance Doshas in to its normal position.- Kashaypa has mentioned following sanshaman chikitsa inAmlapitta.(1) Langhana(2) Laghu bhojana(3) Satmya Kala & Desha Sevana(4) Pachana Karma with Samanyoga* Langhana :-Amlapitta is an Amashayetha Vyadhi so langana has role for it.Charaka said that Amavisha is produced by Ajirna which responsiblefor Amlapitta Langhana is best receipie for removing the Ama Doshaand Ajirna, Langhana in crease the Agni and so, the root cause ofAmlapitta will be ruled out.* Laghu Bhojana :-If the Ahara that taken by the pition digest easily it is called aslaghu bhojana. Laghu Bhojana are not creat Mandagi and Ajirna. 67   
  • * Satmaya kala & Desha sevana :-For the pt. of Amlapitta, sharad Ritu, varsha ritu and Anupa Deshaare Astmya these seasions and Desha are responsible foraggravation if the dis. process. So, releving of these factors must benecessary. They lead to exaggarate the pitta Dosha63.* Pachana Karma with shamana Yoga :-Ama pachana is necessary in Amlapitta. Pachana karma has also arole of Agni vriddhi becasue of same drugs like sunthi, patolapatra,Guduchi, Amlaki, etc have a Deepana & pachana both property.According to Kashyap –a. Since the disease is stomach oriented, and Kapha Pitta are thedominating Dosha, Vamana should be first administered.b. After Vamana, Shamana drugs should be used. At the same timePachana drugs should be given.c. When the Samsarga Doshas are elevated and stomach becomesclear, deepana drugs should be administered.d. If Doshas have shifted into pakwashaya, virechana andshamasana drugs should be used to eliminate the dhoshas.Drugs used in Amlapittaa. Common drugs (herbal)Ativivisha Shatavari ParpatakaMusta Amalaki DhanyakaTrayamana Yastimadhu HinguPatola Bhringaraja NarikelaGuduchi Vasa KusmandaKiratatikta Nimba YavasaTrivrita Pippali ArkaTriphala (Haritaki) Rasana VidangaDanti Udumbara Draksha 68   
  • b. Rasa DravyasShankha Shilajita ShuktiAbhraka Mandoora SwarnaLauha Raupya GandhakaSwarnamakshika Parada VaratikaKaparda Manahshilac. Famous Recipes Bhunimbadi Kwath, Shhatavari Mandura, Varunadi Kwath,Mandura, Narikela Khanda, Shatavari Ghrita, Kushmanda Avaleha,Ghrita, Kamdugdha Rasa, Avipattikara Chura, Sutashekhara Rasa,Lilavilas Rasa, etc.Pathya Apathya –The following list of pathya apathyas found in the disease Amlapittais suggested by various ayurvedic scholars.Ahara –i. Annavarga – Yava, Godhuma, Purna Sali, Mudga Yusha, LajjaSaktu.ii. Saka varga – Karavellaka, Patola, Kushmanda etc.iii. Phala Varga – Dadima, Amalaki, Kapittha, Mrudivika, etc.iv. Dugdha varga – Godugdhav. Mamsavarga – Jangala, MamsarasaVi. Haritvarga – Palandu, Pipali, Haritakivii. Miscellaneous – Sarkara, Madhu, Marikela UdakaVihara –Shitopachara, Vishrama etc.Apathya –i) Ahara – Guru, Vidahi, Viruddha, Kulatha, Udada, Navanna, Tila,Fermented Foods Like Bread.ii) Vihara – Vegavidharana, Atapasevena, Chinta, Krodha, Shoka 69   
  • MODERN REVIEWAnatomy of stomach Stomach is the most dilated part of the digestive tube. It liesin the epigastric, deft hypochondrium & Umbilical regions, the basicAnatomical subdivisions of the stomach correlated with histologicalappearance of Gastric mucosa in different regions. (D1, D2, D3, D4are the 1st to 4th position of Duodenum.) can be seen in fig64.Histology65: - The wall of the stomach consists of 4 layers-i) Serous, ii) Muscular, iii) Sub mucus iv) Mucus.j) Serous Layer: - this layer covers the entire surface of the organ, except (i) along the attachment of greater & lesser omenta (ii) the base area close to the cardiac orifice.ii) Muscular layer:- This layer consists of 3 layers of unstripedmuscle fibres longitudinal, circular or oblique.iii) Sub mucus layer:- It consists of loose areolar tissue.a) Mucus layer:- It is thick & it’s surface is smooth & velvety. There are 6 types of cell in gastric glands. 70   
  • b) The surface cell:- The surface epithelial cell contain abundant musous granules and are designed to protect the epithelium from gastric acids.c) The neck cell:- It lines the entrance of the gastric glands. These also buffer the acid as it enters the gastric pit,d) Chief cells (Zygomatic cell):- These cel contain coarse granules pepsinogen.e) Progenitor cell (Stem cell):- These are concerned with the development of new surface cell and the cells of the gastric glands.f) Parietal cells (Oxyntic cell):- Thses are larger cells and secrete HCI of the gastric juice.F) Endocrine cell:- These cell secrete Gastrin and Serotanin.Blood supply: - Mainly the Left & right Gastric artery, the Left &right gastroepiploic vein.Venous drainage:- The venous of the stomach ultimately turns intothe portal vein.Nerve supply66:- i) Sympathatic ii) Para Sympathetic supply is via Vagus.Sympathetic stimulation causes i) Vasoconstriction of gastric bloodvessels.ii) Relaxation of gastric muscles.The position of Prasympathetic stimulation. 71   
  • G cell- gastrin- parietal cell- HCIStimualtion vagal fibers Direct stimulation- parietal cell- HCI Leads to stimulation ECl – Histamine- parietal cell – HCI Mucius cell- mucus Chief cell- pepsin. Vagal parasympathetic stimulation cause rise of HCIsecretation by- a) direct stimulation of parietal cell. b) Inhibition ofsomatostain secretion. c) via Gastrin release peptide stimulation ofGastric secretion. d) stimulation of Histamine secretion.Gastric secretions67:- A) The HCI B) Harmone Gastrin C) Pepsin D)Mucus E) intrinsic factor F) Bicarbonbate ions (HCO3).The Gastric Juice:-Definition:- It is mixture of gastric secretion.Volume :- 24 hrs, the volume of secretion is between 1 to 1.5 liter.PH:- The PH of the whole gastric juice varies from about 1.5 to 6 inhealthy persons, usually.Ingredients: - Liquid- 99.45% of the gastric juice is water.Solid: - 1) In organic (0.15%) a) The HCI b) The bicarbonates.2) Organic- a) The enzymes b) Mucus c) Intrinsic factor isstrongly acidic with PH – 0.9 to 1.5. 72   
  • Functions of the individual compounds of the gastricsecretions.Secretions Function1) HCI i) Conversion of pepsinogen to pepsin. ii) Bacteriostatic action. ii) It stimulates secretions of some GI harmones. iv) Denaturation of food which reners them more easily digestable. v) Fascilitating absorption of iron by covering colliodal iron into ionic form. vi) Stimulates duodenum to libreate secretion.2) Pepsinogen i) Powerfully digested food in the combination of acid.3) Mucus i) Protects the gastric mucosa. ii) Combine with HCO3 & act as a mucosal barrier. ii) Absorption of oral in injected vitamin.Stimulation of HCI secretions68Stimulation ActionHistamine (H) It combine with Histamine receptor (H2) on the parietal cell and stimulate parietal cell to secrete HCI.Gastrin (G) By direct stimulation of parietal cells & by stimulation of histamine release from enterochromaffin like cells.Acetyl Choline It combine with ACH receptor of the parietal cell(ACH) leading to parietal cell stimulation to secrete HCI. 73   
  • Inhibition of HCL Secretions69.Inhibation ActionProstaglandions It act through inhibilary G proteins that decrease the generation of cyclinic adenosine monophosphateSomatostain By paracrine effects & directly inhibits ‘G’ cells inturn Gastric secretion inhibited.Acid chyme When came in contact with the Duodenum secretin is secreted & it also intiated a reflex which inhibit HCI secretions.Fat i) Fat releases gastric inhibitary peptide which inhibits gastric release as well as directly inhibits parietal cell to secrete HCI. ii) It causes release of Enterogastrone which suppresses HCI secretion.Phases of Gastric secretion & their regulation70 74   
  • Effect of Drug on Gastric acid secretion71Reduction Neutralization1) H2 antihistamines : Antacid-i) Climetidine, ii) Famotidine etc. a) Systemic: I) Sodium bicarbonate2) Proton Pump inhibitor- b) Non Systemic – Mag. Hydroxide,1) Omeprazole, Lansoprazole Mag.trisilicate3) Anticholinergics-i) Pirenzepine ii) Propantheline4) Prostaglardi analogues:-Misoprostol, Enprostil.Measures to control Gastric acidity.No Mesurersa) Neutralizing Gastric acid using Anatacids.b) Inhibiting Gastric acid secretion with drugs.c) Cessation of smokingd) Withdrawl of Gastric acid secretion stimulants such as alcohol, caffeine & soft cold drinks.e) Surgical treatment such as partial Gastroctomy or Vagotomy 75   
  • MODERN VIEW It is very much essential to co-relate the disease which arementioned in the classics with the recent disease of modernmedicine for a better comprehension of the pathogenesis. Inmodern medical literature, some technical terms have been used toindicate an abnormal condition resembling to Amlapitta. Theseterms either explain the pathological condition of the disease orexplain the characteristics of the disease. It is very difficult to co-relate Amlapitta with a single disease entitity of modern science.Following is the opinion of scholars till date.YEAR SCHOLAR DISEASE CO RELATED1962 Tripathi Gastritis syndrome1968 4th national seminar on Ayurveda i. Sri Purushottam Vaidya Acute Gastritis (Pitta vitiation) ii. Vd. Vishwanath Dwivedi Chronic gastritis1982 Tripathi S N Non – ulcer dyspepsia1986 Harinath Jha Hyperacidity Also a conference of Vaidyas held at Hrishikesh, has decidedthe condition like hyperacidity, hypoacidity, gastritis, gastricatrophy, gastric and peptic ulcer, gastric carcinoma etc., can beincluded in Amlapitta.Hyperacidity – This word is composed of two components i.e.hyper and acidus. Hyper means over or excess and acidus meanssour. So a straight meaning may be derived as excess of acid i.e. 76   
  • any acid not particularly the HCl in stomach and a disease whichcontains this abnormal pathology is defined as hyperacidity.Hyperchlorhydira – This indicates the condition in which there isan excessive production of HCl in the stomach. It is a characteristicobservation in certain forms of dyspepsia particularly associatedwith duodenal ulcer. It causes heartburn and water brash.Dyspepsia – Indigestion is a collective term for non specificsymptoms though to have originated from the upper GI tract.Symptoms –i) Upper abdominal pain or lower chest pain with or withoutrelation to food.ii) Regurgitationiii) Heart burniv) Water brashv) Anorexiavi) Nauseavii) Vomitingviii) Bloating, belching, flatulenceix) Early repletion (satiety after meal)A research programme conducted at Banaras Hindu University,Varanasi by S. N. Tripathi and R. N. Mishra (1962) have brought anew concept that patients have been both hyper andhypochlorhydria shows the same sign and symptom of Amlapitta.And they have concluded that Amlapitta is nothing but gastritissyndrome.Gastritis syndrome –Gastritis means inflammation of gastricmucosa where as syndrome means a condition which is associatedwith different types of symptoms. The term refers to the nature of 77   
  • the disease as an assemble of symptoms resulting out ofpathophysiological condition of the stomach.Gastritis – Gastritis refer to inflammation of the gastric mucosawhich is not a single disease but rather a group of disorder that allinduce inflammatory changes, differ in their clinical features,histological characteristics and causative mechanism. Severalclassifications are as below –Classification of Gastritis72A) ACUTE GASTRITIS 1) Acute H. Pylory gastritis 2) Other acute infective gastritis (bacteria, viruses, fungi, Parasites) 3) Actue non- infective gastritisA) 1) Type A (autoimmune) : Body-fundic predominant 2) Type B (H. pylori- related) : Antral-predominant 3)Type AB (environmental): Antral-body gastritis 4) Chemical (reflux) gastritis : Antral bodyu predominant 5) Uncommon forms of gastritisAcute Gastritis73 :- It consists of a sudden derangement ofdigestion due to inflammation of the mucosa of the stomach.Aetiopathogenesis74 1) Diet & personal habits : a) Highlyspiced food b) Excessive alcohol consumption c) Malnutrition d)Heavy smoking e) Excessive quantity of normal food.2) Infections :- a) Bacterial eg H. Pylori b) Viral – eg. Viralhepatitis.3) Drugs:- Intake of drug like Aspirin, Cortisone, Phenylbutazone,Indomethacin, prepartions of iron, chemotherapeutic agents. 78   
  • 4) Chemical & physical agents :- a) Intake of corrosive chemical& Physical agents such as Caustic soda, Phenol, Lysol. b) Gastricirradiation c) Freezing.5) Severe stress :- a) Emotional factors like shock, anger,resentment etc. b) Extensive burns c) Trauma c) Surgery.Prognosis75 :- Recovery generally takes place in about 3 to 6 days.It may go on to chronic Gastritis.Symptoms76 :- 1) Pain, intense & burning or a feeling of distention in the epigastrium, coming on directly after food & accompanied by tenderness on pressure. 2) Vomiting not always immediately after a meal, of undigested food & mucus, sometimes with streaks of blood. 3) Malise, anorexia, slight pyrexia, headache, depression, other constitutional symptoms may be present. 4) Diarrhoea may ensure after a day or two. 5) Accompaining either local disease of the stomach or Cholecystitis, Gall stones & chronic Pancreatitis. 6) Acute or chronic febrile illness.Treatment77 :- a) Management of cause specially chemotherapy for actueinfections, antidotes for corrosive poisons. b)Diet- mainly fluids c)Drugs- Antiemetics like triflupromazine- IM for vomiting, sedatives,IV fluids if required.Chronic Gastritis78 :- It is a common form chronic Dyspepsia. It was formerly calledas atonic or nervous dyspepsia. 79   
  • Causes:- 1) Due to excessive consumption of tobacco, alcohol & hot drinks. 2) Acute Gastritis may go on to chronic Gastritis.Symptoms:- 1) Pain or distress usually in the epigastrium. 2) The appetiteis usually diminished, it may be good but ceases quickly afterbeginning the meal. 3) Bad taste in the mouth, the tongue isflabby, dry & indented by the teeth. 4) There is tendency toeructation & heart burn, nausea, even vomitting may occur but notfrequently. 5) There are languor, headache, depression, disturbedsleep, fatigue, discomfort & drowsiness after meals. There may bepalpitation dyspnoea & other cardiac symptoms sometimes acnerosacea & urticaria.Description & types of chronic Gastritis:-A) Types A Gastritis (Autoimmune Gastritis)79 :- It involvesmainly the body fundic mucosa. It is also called autoimmuneGastritis due to the presence of circulationg antibodies and issometimes associated with other autoimmune diseases likeHashimoto’s thyroids & Addisons diseases. As a result of antibodiesagainst parietal cell & intrinsic factor there is depletion of parietalcell & impaired secretion of intrinsic factor due to which there maybe Gastric atrophy or pernicious anaemia.A) Type B Gastritis (H. pylori related)80 :- This is more commonand mainly involves the region of antral mucosa. It is also called asHyperscretary Gastritis due to excessive secretion of acid,commonly due to infection with H. pylori. 80   
  • B) Type AB Gastritis81:- This Gastritis affects the mucosal regionof A as well as B type & is most common type of Gastrits in all agegroup. This is also called as environmental Gastritis because anumber of as yet unidentified environmental factors have beenimplicated in its aetopathogenesis and chronic Atopic Gastritisbecause in advanced stage, there is progression from chronicsuperficial Gastritis to chronic Atrophic Gastritis.C) Alcoholi Gastritis82 :- It is produced by persistent dieteticerrors, especially alcoholic excesses and is aggravated by thechange in the esophagus and venous congest on arising fromcirrhosis of the liver.E) Erosive Gastritis83 :- This is caused by agents which disturbsthe gastric mucosal barrier. NSAID’s & alcohol are common causes.F) Acid Gastritis84 :- It is also called as Acid dyspepsia orHypochlorhydria.Causes:- It is due to causes which bring about directly or reflexexcessive secretion of gastric juice or retention with pyloric spasm.Among these are- 1) Nervous strain & worry especially business strees from travelling & interview 2) Alcohol 3) Tobacco & condiments. 4) Diseases like Colitis, Appendicitis, Cholelithiasis, Gastric or Duodenal ulcer & duodenal diverticulum. The Patients complains of bouts of indigestion in which thediscomfort does not come on soon after a meal, is followed by 81   
  • vomiting of acid fluid & is relived by food & by alkalies. Thediscomfort consists of sinking feeling in the epigastrium or hungerpains. The disease is probably Acid Gastritis.G) Diagnosis of chronic Gastritis85 :- A) test meal b)Gastroscopy c) X-ray Examination.H) Prognosis of chronic Gastritis86 :- it depends on the cause &duration of the symptom. It is never fatal, but often renders lifewretched for the sufferer.Treatment87 :- 1) Bed in acute cases with servers pain. Gastric lavage & hot packs. 2) Elimination of passible causes like alcohol, spices, hot foods, mastication of food unlcerogenic drugs to be avoided. 3) Treatment of Anaemia in long stading Gastritis. 4) For Achorhydria- 12 tsf of dilute HCI in glass of fruit juice sipped with meals. 5) For pain:- Ulcer regimen with small feeds. 6) For bleeding:- Ice water lavage & other measures for treatment of hematemesis. 82   
  • Consequences of long term H. Pylori Gastritis88Description of diagnostic Test:-Gastric Analysis Test Gastric analysis denotes an examination of the gastriccontents at various phases of digestion. Rehfuss in 1914 introduced a method for Gastric analysis orFractional test meal which once upon a time was very popular androutinely done in cases of Peptic ulcer to see whether there wasHyperacidity or Hypoacidity or Achlorhydria and so on89. This is rather old and not used these days. Gastric analysisinvolves the collection of stomach contents by Ryles tube in fasting.This is followed by a gastric stimulation, giving a test meal (wheatbread, rice gruel etc.). The stomach contents are aspirated by Rylestube at different time periods (usually every 15 min. for 2/12 hrs.)the samples are analysed for free & total acidity90.Indications91 :- There tests are worth performing in followingconditions. 1) For the diagnosis of disease of the stomach and Duodenum.. 2) In clinically suspected cases of Zollinger Ellison syndrome, Gastric atrophy, Menetriers disease. 83   
  • 3) The postvagotomy subjects to assesses the completeness of Vagotomy. 4) For detection of TB in case of pulmonary tuberculosis in children.Contradindications92:- (To gastric intubation) 1) Patient’s with Oesophageal varices, Diverticula stenosis or malignant neoplasme & Oesophagus. 2) Aortic apeurysm. Recent severe gastric haemorrhoge. 3) C. C. F., pregency.The following information may be obtained93 :-A) Information about gastric functioning.-1) Secretary function:- a) Acid secretion b) Enzyme secretion2) Motor function:- Resting juice volume, presence of foodparticles emptying time of the test meal.B) Information about intragastric disease:-a) Presence of blood (Macroscopic, Macroscopic occult) b) Gastricmucus (In abnormal quantity) c) Exfoliated epithelia (In a large no.)d) Micro organisms e) Tissue fragments etc.C) Information about extragastric disease:- a. Bile in the residum, constant regurgitation during Gastric aspiration. b. Swallowed Blood, pus mucus. c. Bile staining of exfoliated billary tract, Epithelia, blood cell, pus cells, mucus, micro organism.Procedure94 :-A) Instruction:- 84   
  • 1) The patient should instruct to take a meal 12 hrs. Preceding the examination. 2) The teeth should not be brushed on the morning of examination to exclude any possibitlity of swallowing blood. 3) The patient is adviced not to taken antacid or anticholinegic drags for previous 24 hrs. 4) The patient is posted with the information regarding intubation & assured with his cooperation being soughty for.B) Withdrawl of gastric contents:- The gastric fluid is obtainedby aspiration through a nasogastric tube. The best recover gastricsecretation is obtained with the patient, in sitting, position patient’snostril and throat are sprayed with a solution of 3% Lignocaine inisotonic solution. A nasogastric tube which was ryles tube previouslyand now it is plastic radio opaque 125cm. long tube with holes closeto the tip is first well lubricated with liquied paraffin & is passedthrough the nose. The pt. is asked to swallow repeatedly while thetube is being pushed steadily and rapidly down through the pharynxand esophagus into the stomach. When a total of about 56cm. oftube has been pushed the tip is in the stomach, it is confirmed byaspiration of gastric juice.C) Aspiration of fasting sample: - 20 ml syringe attached to thetube & gastric contents should completely emptied by aspiration.The sample is labelled as ‘fasting’ Washing the stomach with about20 ml. of distilled water, ensures complete emptying, this washingsample is not included in the fasting sample. E) Administration of test meal :- A test meal is a meal containing material given for a specific purpose for aiding 85   
  • diagnostic examination of stomach by roentgenoscopy or by chemical analysis later of gastric contents. In this clinical study we adopted ewald test meal in whichplain wheat bread 35gr. And water 300 to 400 ml is given throughthe mouth95. An hours later the stomach contents were removedcompletely, gastric content is gently aspirated after 15 min., about10 ml is collected in a clean dry test tube. The procedure isrepeated every 15 min. & 10 samples are collected.96Examination of gastric contents97 :- Routinely the samples areexamine as follows.Macroscopic of gastric contents:- 1) Volume: Normally 20-50ml. 2) Colour: Generally colorless. It may be Green or Yellow done to the presence of bile or blood. 3) Odour: Normally odourless under pathological contition it may be sour as rancid, may foul in cases of Caricinoma of Stomach. 4) Consistency: It is normally a clear fluid. It may become viscous done to the prescence of mucus or undigested food. 5) Bile: It is generally adsent but may appear due to regurgitation. 6) Blood: Normally absent. If present it can be detected by Benzidine test. 7) Starch: Generally absent in fasting sample. It may be present due to undigested food. 86   
  • Chemical Examiantion:- HCI of the Gastric juice is the componentof chief diagnostic intrest. The juice in addition to other constituentscontains free HCI. It makes the reaction of the gastric juicemarkedly acidic. Chemical examination of gastric contents both thefasting, interdigestive as well as after test meals are of paramountimportance. These examination includes test for free acid totalacid98.A protion of the acid combines with proteins or protein likesubstances. The protein salts of HCI so formed are known ascombined acid. The HCI which remains in excess is known as freeacid of free HCI.Total acid:- It is defined as the amount of standard alkali requiredto titrate 100ml. of gastric juice to PH 8.5 The peak total aciditymay be as high as 70-80ml.99Normal100 :- Total acid- 10 to 50 cu or degrees or m.Eq/LAverage:- 30 cu or degrees or m. Eq/LFree acid101 :- It is defined as the amount of standard alkalirequired to titrate 100ml. of Gastric juice up to PH 35. Normally infasting sample it is only 10-20ml. It increases & reaches with apeak value one hour after the test meal. It remains high for half anhour. The acid level comes back to the resting level within 3 hours.Normal102 :- Free HCI 0 to 30 cu. Or degrees & m. Eq/LAverage - 18.5cu or degrees or m. Eq/LCombined acidity103:- The portion between total acidity & freeacidity curves indicate combined acidity. 87   
  • Example:- For 10 ml of the gastic juice 3.2 ml. of 0.1 N NaOHrequired with the Tofers indicator & 3.9 ml. (including 3.2 ml of thefirst titration) are required with Phenopthalein.Free acidity - 3.2×10=ml. (32x3.65=116.8mg HCI) i.e.32.m.Eq/L.Total acidity - 3.9x10=39ml, (39x3.65= 142. 35 mg HCI) i.e 39ml. m.Eq/LCombined - 39-32=7ml.acidity 7x3.65=25.55 mg. HCI i.e.7Eq/LGastric Analysis Test Limitaions:- A properly performed gastricanalysis requires a relatively large investment of time by thephysician who must perform the intubion & supervise the collectionof specimen. Although the procedure is begin experience, intubationis apt to be unpleasant & sometimes traumatic for the patients. Inview of these facts and the inherent limitations of the informationgain through Gastric analysis. It is performed infrequently at thepresent time. Gastroscopy, Roentgenography & Gastric cytology arefor more useful in establishing the diagnosis of Gastric pathologythan in gastric analysis. 88   
  • Drakshya Raisin 89   
  • Haritaki HirdaSharkara 90   
  • DRUG REVIEW The Ayurveda believes in maintaining the balance of Tridoshain the body to keep person healthy. The effect of certain Ayurvedicpreparations with the concerned vyadhihara Dravyas has beenexplained with their therapeutic literature. The pharmaco-dynamics of these drugs & their compoundpreparation has been explained on the basis of Rasa, Guna, Virya,Vipaka & Prabhava. An Ayurveda drug or diet or diet articles thatreverse or break the samprapti without producing any side effecthas been looked upon as ideal drugs or diets. It has been well said by Acharya Charaka a drug that is notunderstood perfectly is comparable to poision weapons, fire and thethunderbolt-while the perfectly understood drug is comparable toambrosia. The word drug is derived from the French work ‘Drogue’ whichmeans dry herb, drug as defined by who is a substance or productthat is used or intended to be used to modify or explore thephysiological systems or pathological states for the benefits of therecipient. The best drug is that which cures the disease promptly & alsopreserve or sustains the health of an individuals. It is the single active chemical entity present in a medicinethat is used for diagnosis in a medicine that is used for diagnosisprevention treatment cure of a disease104. 91   
  • The drug which are having Tikta & Madhura – rasa, sheetavirya & vatu-Vipaka Laghu & Ruksha property. On the basis of above description ‘Drakshadi Gutika’ wasselected of its contents are having following property.DRAKSHYADI GUTIKAReference : Bharat Bheshajya RatnakaraIt contains the following drugs & All drugs taken into equal quantity.Drakshya Churna: Vitis Vinifera, Linn.Haritaki Churna : Terminalia Chebula.Sita (Khand sharkara) : The formation was prepared as per the formulations of thereference. The pts. Were advised for 2 gm TDS. After meal (1 tab will beof 1 gm) sheetal jala as Anupana. The chief properties & pharmacological action of the totaldrugs under trial in the present study alongwith their probableaction on samprapti of the disease Amlapitta & other relevantinformation as discussed below. The detail of contents of Drakshyadi Gutika has beendescribed further.Drug Rasa Virya Vipaka Guna KarmaNameDrakshya Madura Sheeta Madhura Singdha Vatta-pitta Guru Shamaka MriduHaritaki Except Ushna Madhura Laghu tridoshahara Lavana RukshaSita Madhura Sheeta Madhura Guru Vatta-pitta Snigdha Shamaka 92   
  • 1. DRAKSHYA :Botanical Name : Vitis Vinivera Linn.Natural Order/family : Vitaceae.Synonyms : Drakshya, Mridwika, Gostani, Charuphala, Kapisha,Swaduphala.Vernacular Names :Hindi : Munakka, Kishmish.Gujarati : Drakh, Draksha.Panjabi : Munaca, Angur, Dakh.English : Dry grapes, Raisins, wine grape.Marathi : Drakshya, Angur.Part used :Ripe fruit (dried), leaf, stem, flower.Gana :Snehopag, virechanopag, kasahara, jawaraghana (ch.)Kakolyadi, parushadadi (Su.)Rasapanchaka : (Pharmacodynamics)Rasa : MadhuraGuna : shigdha, Guru, Mridu.Virya : SheetaVipaka : MadhuraDoshaghnata : VatapittashamakaChemical constituents : Fruits contain grape-sugar (Glucose) gum, tanin, tartariccitric, racemic & malic acids, chlorides of potassium & sodium, 93   
  • Sulphate of potash, tartrate of lime, magnesia, alum, iron somealbumin. Ozotised matters and acid tartrate of potassium. Tartaric acid is the characteristic acid of the grapes. As o.05mg. in 100 ccm in fruit-juice and oxalic acid in unripe fruits Raisinscontain calcium, magnesium, potassium, phosphorus and iron in anassimilable form besides gum & sugar seeds contain a dense fixedoil or fat & tannic acid 5 p.c. skins contain tanin. Wine contains from7 to 24% of alcohol.Pharmacological Activities : Antifungal, angiotensin, converting enzyme (ACE) activity,tumour inhibitory, Antiulcer, Hepatoprotective, antioxidant, woundhealing antimultagenic, antiherpetic, cardioprotective breast cancersuppressor, antibacterial.Actions & Uses : The fruits are sweet refrigerant, laxative, demulcent intellectpromoting cardiotonic, haematinic, haemostatic diuretic aphrodisiac,rejuvenating nervine tonic, febrifuge depurative, antispasmodic,digestive, stomachic suppurative expectorant & tonic. They areuseful in burning sensation, dipsia, constipation, amentia, cardial,debility, haemoptysis, haemorrhages, anaemia strangury,consumptions & wasting diseases, fever, leprosy, skin diseasesdyspepsia, colic flatulence, cough, asthma, bronchitis, affectionsof eyes and throat Bright’s disease, gout. Jaundice, & generaldebility. The leaves are astringent anodyne, diuretic, depurative anduseful in cephalalgia strangury, scabies skin disease, syphilis,haemorrhoids diarrhea, splenamegaly & vomiting the ash of thestem is good for arthralgia vesical calculi, haemorrhoids & arehitis.Sap young branches is used in skin diseases. The flowers are 94   
  • expectorant. Emmenagogue & haematinic & are useful in bronchitis,liver disorders, anaemia, amenorrhoea & dysmenorrhoea. 2. HARITAKIBotanical name : Terminalia ChebulaNatural order/family : CombrataceaeSynonyms : Haritaki, Abhaya, Pathya, Putana, Haimavati, Chetaki,Shiva, Rohini.Vernacular names :English : Chebulik myrobalanHindi : Harad, pile-har, Hara.Gujrati: Hardo.Bengali : HaritakiMarathi : Hirda, Hirda-phula, Bala hirade.Part used : FruitGana :Prajasthapana, Jwaraghana (Ch.) Triphala, Amlakyadi, Parushakadi(Su.)Rasapanchaka (Pharmacodynamics) :Rasa : Kashaya, Tikta, Madhura, Katu. Amla.Guna : Laghu, Ruksha.Virya : UshnaVipaka : MadhuraPrabhava : TridoshashamakaDoshaghnata : Tridoshashamaka 95   
  • Rogaghnata : Vatavyadhi, shotha-vedanayuktavikara, Vrana, Mukharoga,Kantharoga, Nadidaurbalya, Mastishka daurbalya, Netrabhishyanda,Drishtimandya, Indriyadaurbalya, Agnimandya, Shoola, Anaha,Gulma, Vibandha, Udararoga, Arsha, Kamala, Yakritplee havridhi,krimiroga Hriddaurbalya, vatarakta, Raktavikara, Shotha,pratishyaya, Kasa, Swarabheda, Hikka, Shwasa, Prameha,Shukrameha, Shwetapradara, Mootraghata, Ashmari, Prameha,Kushta, Visarpa, Twagoosha, Vishamaj wara, Jeerna Jwara.Karma : Shothahara, Vedanasthapana, Vranashothan, Vranoropana,Nadibalya, Medhya, Chakshushya, Deepana, Pachana,Yakriduttejaka, Anulomana, mridurechana, Krimighna, Grahi,Shonitasthapm, Hridya, kaphaghna, Srotah-Shodhana, Vrishya,Garbhashayashothahara, Prajasthapana, Mootrala, Kushthaghna,Rasayana.Doses : 3-6 gmChemical Constituents : Anthraquinone glycoside, Chebulic acid chebulagic acid, tunicacid terchebin, tetrachebulin, Vitamin C (fruits), arachidic, beheniclinoteic, oleic, palmitic & stearic acids (fruit hernels), Chebulin(flowers). 2 hydroxymicro meric acid, maslinic acid & 2 hydroxyursolic acid (leaves).Pharmacological Activities : Antimicrobial, antifungal, Antibacterial antistress,antispasmodic, hypotensive, indurance, promoting activity, antihepatitis B virus activity, hypolipidaemic, inhibitory activity againstHIV-1 protease, anthelmintic; purgative. 96   
  • Actions & Uses : Fruits are astringent, sweet, acrid, bitter, sour, themogenic,anodyne, anti-inflammatory, vulnerary, alterant, stomachic,laxative, purgative, carminative, digestive, anthelmintic dentifrice,cardiotonic, aphrodisiac, antiseptic, diuretic, febrifuge depurative &tonic. They are useful in wounds ulcers inflammations, skindiseases, leprosy stomatitis, hyperacidity & associated gastricdisorder, anorexia, indigestion, flafulence, constipation,haemorrhoids. Jaundice hepato-splenomegaly, other abdominaldiseases, helminthiasis, anaemia, delirium, pharyngitis, hiccough,dyspnoea, cough, coryza, asthma, scrotal, enlargement, urinarydisorders, vesical & renal calculi, soft chancre, seminal defects,cephalagia, narcosis, fainting, epilepsy, ophthalmic diseases,intermittent, fevers, cardiae disorders filoria, obesity, neuropathyrheumatoid arthritis, whitlow, dandruff, general debility. In combination & phyllanthus emblica & Terminalia belliricaunder the name Triphala fruits of Terminalia chebula are extensivelyused as adjunct to other medicines in almost all diseases. 3.Sita (Khand Sharkara)105Synonyms SHARKARAAyurvedic Properties:-Rasa:- Madhura.Guna:- Guru, Snigdha.Virya:- Sheeta.Vipaka:- Madhura.Doshaghnata:- Vata pitta shamaka.Chemical Constituents:- Glucose, fructose and sucrose.Uses:- Vata pitta shamaka, Raktashodhaka and used in Raktajaroga. 97   
  • PLACEBO Placebo is a Latin term which means, “I may please you.” Theplacebo effect is an effect attributable to a medicament as aprocedure & is not due to any specific pharmacodynamic property ofthe substance for the condition being treated. Placebo effect may bedefined as “how the patient’s perception of treatment influenceshis/her response.”106. This is an inert substance which is given in the garb of amedicine. It works by psychological rather than pharmacologicalmeans & often produces responses equivalent to the active drugsome individuals are more suggestible & easily respond to aplacebo- ‘placebo reactors’ placebos are used in two situations:A) As a control device in clinical trial of drugs (dummy medication)B) To treat a patient who, in the opinion of the physician does notrequire an active drug placebo is a Latin word meaning. I shallplease. A patient responds to the whole therapeutic setting placebo-effect largely depends on the physician patient relationship. Placebo do induce physiological responses e.g. they canrelaease, endorphins in brain-causing analgesia. Naloxone an opiodantagonist, blocks. Placebo analgesia placebo effects can thussupplement. Pharmacological effects. However placebo effects are highlyvariable even in the same individual e.g. a placebo may inducesleep on the first night but not subsequently. Thus it has overylimited role in practical therapeatics substances commonly used asplacebo are lactose tablets/ capsules & distilled water injection107. 98   
  • As therapeutic agents that work psychologically. A placebo preparation is usually an inert substance like starchor lactose A supportive physician-patient relationship generally ispreferable to the use of a placebo for promoting therapeuticbenefits Relief or lack of relief of symptoms upon administration of aplacebo is not a reliable basis for determining whether thesymptoms have a “psychogenic” or “somatic” origin. Placebos can often produce relief of subjective symptomsassociated with psychological disturbances. This includes relief fromanxiety, headache, pain, insomnia, & breathlessness. Hencepacebosare often employed in the treatment of certain diseaseswhere the psychic element is suspected to be responsible forsubjective symptoms objective responses such as increase ordecrease in neutrophills In eosinophils may sometimes be seen withplacebos. When administered for its therapeutic effects the placebopreparation.  Must appear to be relevant to the illness.  Must be harmless &  Should preferably conform to the patients’ expectations. To be effective, the ‘potency’ of the preparation must beshown by some sings such as strong taste, a colorful capsule or atable of odd shape & sometimes even by obvious but harmless sideeffect like coloured urine. During clinical trials, placebos are used to eliminate the effectof bias of the physician & patient, particularly in evaluating a newdrug claimed to be effective in conditions like bronchial asthma,angina pectoris, and pain & psychiatric disorders. In such cases the 99   
  • placebo should be indistinguishable form the active medicament inphysical properties like colour, smell taste & form. Placebo effect may be modified by:- Personality of the physician-Reassurance & optimistic outlookoffer achieve a better effect. “The doctor himself must inspireconfidence. It is difficult to define this quality. It does not lie somuch in what is said as in the doctor’s shape & bearing & in thoseinstinetive signs whereby one animal unknowingly conveys its moodto another. Some have it & some do not. In this respect the hospitalspecialist is an easier postion than the GPbecause he is backed by atemple of healing which is cleary nearer the seat of power than awayside shrine. Since few doctors are good enough actors tosimulate the confidence they do not have it often happens that onewho is kind & credulous is a better healer than another who isinformed and critical placebo reactions go faster when both partieshave faith & in this respect knowledge is an inhibitor. It follows thatanyone who wants to know whether a cure was due to a drug andtherefore reproducible would have to observe the ceremonyconducted by sceptics”. Personality of the patient: some individuals are amenable to suggestions such people are termed placebo reactors, & since a placebo acts by suggestion. They derive benefit from the use of placebos. Neurotics are great placebo reactors. While depressed or psychotic subjects are usually resistant.Individuals who are of conservative, suspicious or sceptical natureare not likely to benefit from placebos. Such negative reactors, onthe contrary, may become. Worse as per their own expectations. A 100   
  • strong negative reactor may even take a pride in saying that he orshe is “allergic to all drugs”. Form of administration: it is not surprising that the greatestplacebo effect (as high as 81.7) is achieve with injections. This mayperhaps explain the preference for the use of injections by thepractitioners colour, taste presence or absence of stress are therefactors which modify placebo effect. Like active drugs, placebos can produce certain adverse.Subjective reaction such as drowsiness, headache, dryness ofmouth, fatigue, insomnia, constipation, impotence, difficulty inconcentrating & impotence, difficulty in concerntrating & a“drugged feeling”. An abstinence syndrome which responds toinjection of normal saline, has been describe after prolongedplacebo therapy. Much of the routine treatment such as vitamins,tranquiliollisers & tonics prescribed by the doctors often acts as aplacebo for themselves too many phycians cannot “bear to thinkthey are doing nothing, so they like their patients are willing tobelieve. They persuade themselves or are persuaded of the virtuesof their treatment.Interpretation of clinical results: After the completion of the clinical trial, the results aresubjected to statistical analysis If the difference between the twogroups of treatment is so large that the probability of its occurrencesimply by chance is less than 5 times in 100 (P<0.05), then thenew drug is said to have produced a significant effect. It isnecessary, however, to rule out all other possible explanations ofrsuch difference, before the verdict is accepted. Various statistical designs have been suggested to ensure thatthe results obtained are as precise as possible without muchinterference by other biological factors & individual bias & their is no 101   
  • doubt that such statistical safeguards are essential. Howeverelaborate statistic cannot validate a poorly designed and executedclinical trial further, in a given study it is more important to knowwhether a new drug is significantly better than the older one orplacebo in terms of its “clinical effect” & not merely statistically. Infact, on effect whose reality is revealed only after elaboratestatistics is hardly likely to be clinically important. “Statistical significance” & therapeutic significance” of resultsare not necessarily equivalent. Many times statistics would show ‘astatistically significant difference’ but is cannot tell whether suchdifference really matters in therapeutics. Thus, drug may lower theplasma cholesterol concentration statistically but may not preventcardiac infarction. Most of the new drugs are not ‘wonder drugs’ & need properclinical assessment. Unfortunately, because of various factors thequality of many clinical trials is for from satisfactory As pointed outby the lancet, there is no doubt that a prior design of the trial isimportant but “It is clearly not worth devoting such energy to trialdasing. If the trained observer is not both trained and observing.After all, the controlled trial requires as much in ‘clinicalobservation’ as it does in design No. one should play at clinicaltrials” . As pointed out by park house, “A good trial of a poor drug is agreat deal better than no trial at all . It is infinitely better than apoor trial of a poor drug.” Event the use of double blind techniquedoes not guarantee valid. Results in an otherwise poorly designed &executed study. 102   
  • CLINICAL STUDY Clinical contrive 25-30% people are suffering from dyspepsia.These diseases are chronic in nature & affecting to adults mostly.Patients of gastritis aften results into peptic ulcer. Our Ayurvedic classics say that Uradhavaga & AdhogaAmlapitta can be misdiagnosed as Chaardi & Atisara respectively. These disease are caused due to Pittolvana Sannipata withAvarna of vata Ushna. Tikshna, Katu, Amla, Guna of pitta GuruSheeta manda Guna of Kapha & Chala Ruksha Guna of vata ismainly involved. The Avarana of vata should be considered. TheRakta which is also There as dushya & which seems to be mainlyresponsible for progression of Amlapitta & its complication must beconsidered while formulating the treatment. Sangraha Granthakarashave explained the line of treatment mainly divided into twoheadings viz. shodhana & shamana. In shaman chikitsa drugs should have Tikta & Madhura rasa.Hence for the present study “Drakshyadi Gutika” is chosen asshamana theorapy to eradicats the disease from root. & previousstudies have shown that no one has worked on this topic. 103   
  • Materials & MethodsClinical trialDesign A prospective randomized open label controlled clinical trialconducted on diagnosed patients.Selection of the subject : The pts of Amlapitta roga attending the OPD & IPD of thehospital were selected. 60 pts. Fulfilling the diagnostic criteria wereselected for the present study. Pts. Were drown by randomsampling technique, irrespective of sex, cast religion & occupation,they were advised to visit the hospital every week for regular checkup & to asses the effect of therapy there by If any patient leavesthe treatment without completing 30 days it will be decleared asdropped out from the research work.Subjective Criteria A) Inclusion Criteria : 1. The pt. presenting with sign & symptoms of Amlapitta as stated in Madhava Samhita & modern test was consider for study. 2. Irrespective of both sex, cast, religion were included. 3. Age above 15 year & below 60 year. 4. Amlapitta patient with and without complication. 5. With chronicity less than 5 year. 6. The presenting clinical features were recorded in term of Ayurvedic & Modern symptoms & signs are as follows. 1. AVIPAK (Indigestion) 2. TIKTA AMLODAGAR (Anorexia) 3. HRUDKANTA DAHA (Heart burn) 4. CHARDI (Vomitting) 5. SHIRORUJA (Headache) 104   
  • B) Exclusion CriteriaThe patient with following types of known cases were excluded fromstudy. a) Gastric ulcer/peptic ulcer. b) Pregnancy c) Gastric carcinoma d) Esophageal varises e) Haematemasis f) Other malignancy g) ZE syndrome.Objective CriteriaInvestigation a) Gastric function test : Free HCL between 25-50 ME q/L & total acidity between 50-70mEq/L was considered for pt. study. b) Laboratory Investigation : Hb% Urine complete Stool (routine) for occult blood.PLAN OF STUDYCriteria for diagnosis : A special proforma was prepared in corporating importantsigns & symptoms of the diseases. At the onset a detailed clinicalhistory was taken & complete physical examination of each patientwas done on the basis of proforma other necessary investigationswere carried out to exclude other pathologies as well as for theassessment of present health status of patients. 105   
  • MANAGEMENT OF THE PATIENTS :Group – A : Patients were treated with “Drakshyadi Gutika.”Group – B : Patients were treated with cap. Placebo. a) Group – AIn this Group 30 pts. Were selectedDose : 2 gm (1 tab. of 1 gm).Kala : TDS (After meal).Anupan : Sheetal jalaDuration : 30 days. b) Group B :In this group 30 pt. were selectedDose : 1 capKala : BD (After meal).Anupan : Sheetal jalaDuration : 30 days.Diet : As the disease is directly connected diet & dietary habits, sopatient himself knows most of the things which exacerbates thedisease hence he tries to avoid those things. But a detailedexplanation regarding the Astavidha Ahara Ayatana & Ashna.Pravicharas was given to all patients & requested them to follow thesame. However, they were asked to avoid too hot, oily, sour, spicyfor fatty food.CONSENT : Written consent of patient was taken before treatment. 106   
  • CRITETERIA FOR ASSESSMENTSubjective CriteriaGeneral symptoms score :Gradation of symptoms.0 1 2 3No symptoms Mild Moderate Severe A) AVIPAKA : a) Patient can’t digest daily even light 3 b) Patient can’t digest routine diet daily 2 c) Patient can’t digest routine diet & suffer from indigestion 2-3 times per week 1 d) No indigestion on routine diet 0 B) TIKTA AMLODGARA a) Severe tikta Amlodgara frequentation Ground 24 hr. 3 b) Amlodgara frequentation in a day 2 c) Amlodgara sometimes in a day 1 d) No Amlodgara at all 0 C) HRUD KANTHA DAHA a) Burning sensation in throat, chest & upper abdomen & does not relief without medicine 3 b) Burning sensation in throat, chest & upper abdomen & relived after digestion of food or Vomitting 2 c) Burning sensation in one or two of the above mentioned area & relived after digestion of the above mentioned area & relived after digestion of food or vomiting. 1 d) No burning sensation at all 0 D) CHARDI a) Frequency of vomiting after every meal or once in day. 3 b) Frequency of vomiting 4 to 5 time per week. 2 c) Frequency of vomiting not more than 1 to 2 in a week 1 d) No vomiting at all 0 107   
  • E) SHIRSHUL a) Shirshul on fasting 3 b) Shirshul relieved by antacid 2 c) Shirshul with meal 1 d) No shirashul at all 0Objective Criteria (Investigational Assessment) 1. CURED : Patient having free HCL<18 MEq/L total acid<30 meq/L & signs & symptoms were completely cured or more than 75 %. 2. Improved : Patient having decreased acid output but not upto normal range & partial i.e. (50 %) relief in sign & symptoms. 3. Unchanged : Patient having no significant change in acid output & does not change in the sign & symptoms were releaved as unchanged. 108   
  • OBSERVATION In this clinical study of Amlapitta total 60 patients wereregistered & categorized into two equal groups. In group A(Drakshyadi Gutika) 30 patients were registered & 30 patients wereregistered in group B (placebo) each patients of both groupsobserved throughly and noted neatly. The observations quoted from here onwards include data of60 registered patients. The observations are analyzed in the form ofchart & graph.Table No. 1Age wise Age group Number of patients Total Percentage (in yr.) Group A Group B20-30 15 20 35 58.3331-40 8 6 14 23.3341-50 5 2 7 11.6651-60 2 2 4 6.66 The table 1 shows the age wise distribution of the samplestudied. It was found that 58.33 % the patients were from 20-30yrs. Age group 23.33 % patients were seen in group of 31-40 yrs.Age & 11.66 % of patients were seen in group of 41-50 yrs. & only6.66 % patients belonged to the age group of 51-60 yrs. Age. 109   
  • Table no. 2Sex wise Number of Sex patients Total Percentage Group A Group BMale 20 16 36 60Female 10 14 24 40 Present statistical data as shown in table 2 reveals thatmaximum i.e. 60 % of patients were males and remaining 40 % ofpatients were females.Table No. 3Religion wise Number of Religion patients Total Percentage Group A Group BHindu 24 25 49 81.66Muslim 2 1 3 5Buddha 4 4 8 13.33 Table 3 shows that 49 patients (81.66 %) were Hindus, 3patients (5 %) were from Muslim & 8 patients (13.33 %) wereBuddha community. 110   
  • Table No. 4Marital status Number of Marital patients Total Percentage status Group A Group BMarried 23 22 45 75Unmarried 7 8 15 25 Table 4 indicates that maximum No. of patients i.e. 45 (75 %)studies in this series were married 15 (25 %) were unmarried.Table No. 5Educational status Number ofEducational Percentage patients Total Status % Group A Group BPrimary 7 6 13 21.66Secondary 10 12 22 36.66Graduate 12 11 23 38.33Illiterate 1 1 2 3.33 It was found that 23 patients (38.33 %) were educated up toGraduate, 22 patients (36.66 %) were educated upto Secondary, 13patients (21.66 %) were educated upto primary level & only 2patients (3.33 %) were Illiterate. 111   
  • Table No. 6Occupation wise Number ofOccupation patients Total Percentage Group A Group BLabour 6 6 12 12House wife 6 8 14 23.33Service 12 9 21 35Student 5 6 11 18.33Farmer 1 1 2 3.33 It was observed that maximum no. of patients 21 patients (35%) were servicemen/women, 14 patients (23.33 %) wereHousewives, 12 patients (20 %) were labours, 11 patients (18.33%) were students & 2 patients (3.33 %) were farmer.Table No. 7Diet wise Number of Diet wise patients Total Percentage Group A Group BVegetarian 9 13 22 36.66Mix 21 17 38 63.33 Table No. 7 reflects the dietary habits of the patients whichindicates that 38 patients (63.33 %) had mixed dietary habit & 22patients (36.66 %) were vegetarians. 112   
  • Table No. 8Prakruti wise Number of Prakruti patients Total Percentage Group A Group BVata-pitta 16 15 31 51.66Pitta-kapha 5 8 13 21.66Vata-kapha 9 7 16 26.66 Table 8 shows Prakruti wise distribution in this series,maximum no. of 31 patients (51.66 %) were having vata-pittaprakruti, 16 patients (26.66 %) were having vata kapha prakruti &13 patients (21.66 %) were having pitta-kapha prukruti.Table No. 9Vyasana wise Number of Vyasana patients Total Percentage Group A Group BAlcohol 8 7 15 25Tea 9 8 17 28.33Coffee 3 2 5 8.33Tobacco 5 5 10 16.66Smoking 5 8 13 21.66 Table 9 shows maximum No. of patients 17 (28.33 %) werehaving vyasana of Tea, 15 patients (25 %) were having the vyasanaof Alcohol, 13 patients (21.66 %) were having the vyasana ofSmoking, 10 patients (16.66 %) were having Tobacco chewers &also 5 patients (8.33 %) were having vyasana of Coffee. 113   
  • Table No. 10Economical wise Number of Economical patients Total Percentage Group A Group BHigher Class 9 8 17 28.33Middle Class 12 15 27 45Lower Class 9 7 16 26.6 The data shown in table 10 suggest that majority i.e. 27patients (45 %) were from Middle Class of society, 17 patients(28.33 %) were from Higher Class of society & only 16 patients(26.66 %) were from Lower Class of Society.Table No. 11Agni wise Number of Agni patients Total Percentage Group A Group BSama - - - -Vishama 7 4 11 18.33Manda 19 21 40 66.66Tikshana 4 5 09 15 It was found that maximum no. of patients 40 (66.66 %)were having Mandagni where as 11 patients (18.33 %) were havingVishamagni, 9 patients (15 %) were having Tikshnagni & no.patients was having Samagni. 114   
  • Table No. 12Koshtha wise Number of Koshtha patients Total Percentage Group A Group BMadhyama 16 17 33 55Krura 5 3 8 13.33Mrudu 9 10 19 31.66 This table highlights the Koshtha wise distribution of thesample studied, 33 patients (55 %) were having MadhyamaKoshtha & 19 patients (31.66 %) were having Mrudu koshtha, while8 patients (13.33 %) were having Krura Koshtha.Table No. 13Satva wise Number of Satva patients Total Percentage Group A Group BPravara 7 5 12 20Madhyama 13 14 27 45Avara 10 11 21 35 Table no. 13 shows that maximum no. of patients i.e. 27patients (45 %) were having Madhyama satva, 21 patients (35 %)were having Avara Satva, while 12 patients (20 %) were havingPravara satva. 115   
  • Table No. 14Satmya wise Number of Satmya patients Total Percentage wise Group A Group BPravara 9 10 19 31.66Madhyama 17 15 32 53.33Avara 4 5 9 15 Table no. 14 shows 32 patients (53.33 %) were havingMadhyama Satmya, 21 patients (31.66 %) were having PravaraSatmya & only 9 patients (15 %) were having Avara Satmya.Table No. 15Sarata wise Number of Sarata patients Total Percentage Group A Group BPravara 6 6 12 20Madhyama 21 22 43 71.67Avara 3 2 5 8.33 Table no. 15 shows Sarata wise distribution of the patients inthis series maximum no. of 43 patients (71.67 %) were havingMadhyama Sarata, 12 patients (20 %) were having Pravara Sarata& only 5 patients (8.33 %) were having Avara Sarata. 116   
  • Table No. 16Samhnana wise Number of Samhnana patients Total Percentage Group A Group BPravara 8 8 16 26.66Madhyama 21 19 40 66.66Avara 1 3 4 6.67 Table no. 16 shows Samhnana wise distribution 40 patients(66.66 %) were having Madhyama Samhnana, 16 patients (26.66%) were having Pravara Samhnana while 4 patients (6.67 %) werehaving Avara Samhnana.Table No. 17Dominance of Rasa wise Number of Dominance patients Total Percentage of Rasa Group A Group BMadhura 5 3 8 13.33Amla 5 6 11 18.33Lavana 4 3 7 11.66Katu 10 11 21 35Tikta 3 4 7 11.66Kashaya 3 3 6 10 Maximum no. of patients i.e. 21 patients (35 %) were havingKatu rasa pradhana Ahara, 11 patients (18.33 %) were having Amlarasa pradhana Ahara, 8 patients (13.33 %) were having madhururasa prdhana Ahara, 7 patients (11.66 %) were having Lavana rasaas well as 7 patients (11.66 %) were having Tikta rasa & and only 6patients (10 %) were having kashaya rasa pradhana Ahara. 117   
  • Table No. 18Amlapitta Bheda wise Number of Amlapitta patients Total Percentage Bheda Group A Group BVataja 4 6 10 16.66Pittaja 18 17 35 58.33Kaphaja 8 7 15 25 Table no. 18 shows 35 patients (58.33 %) were having pittajaAmlapitta, 15 patients (25 %) were having kaphaja Amlapitta &only 10 patients (16.66 %) were having vataja Amlapitta.Table No. 19Predominant Manasa Bhava wisePredominant Number of Manasa patients Total Percentage Bhava Group A Group BChinta 18 19 37 61.66Krodha 13 13 26 43.33Shoka 3 7 10 16.66Bhaya 6 5 11 18.33None 3 3 6 10 As the data reveals that 37 patients (61.66 %) were havingChinta, 26 patients (43.33 %) were having Krodha as predominantmanasa bhavas, 11 patients (18.33 %) were having Bhaya, 10patients (16.66 %) were having shoka. 118   
  • Table No. 20Ahara Shakti wise Number of patients Shakti Total Percentage Group A Group BAbhyavaharanaShaktiParvara 2 3 5 8.33Madhyama 10 12 22 36.66Avara 18 15 33 55Jarana shaktiPravara 1 2 3 5Madhyama 20 16 36 60Avara 9 12 21 35 Maximum number of patients i.e. 55 % were having avaraAbhyavaharana Shakti while 36.66 % were having madhyamaAbhyava harana shakti & 8.33 % were having PravaraAbhyavaharana Shakti. 60 % patients were having Madhyama jarana Shakti while 35% patients were having avara & 5 % patients were having PravaraJarana Shakti.Table No. 21Sleeping Pattern wise Number of Nidra patients Total Percentage Group A Group BAlpa 4 3 7 11.66Samayaka 19 20 39 65Khandit 5 4 9 15Prabhut 2 3 5 8.33 119   
  • The above table shows that maximum no. of patients 65 %were having Samayaka Nidra, 15 % patients were having KhanditNidra, 11.66 % patients were Alpa Nidra & only 8.33 % patientswere having prabhut Nidra.Table No. 22Subjective Criteria wiseComplaints Group A Group B BT AT BT AT No. of % No. % No. % No. % Pts of of of Pts Pts PtsAvipaka 30 100 19 63.33 29 96.66 30 100Tikta 17 56.66 5 16.66 24 80 21 70AmlodgaraHrud Kanta 28 98.33 16 53.33 25 83.33 28 93.33DahaChardi 16 53.33 8 26.66 14 46.66 11 36.66Shirashula 17 56.66 9 30 27 90 27 9001. In Group A Before treatment Avipaka was found in 30 patients(100 %) while After treatment Avipaka is reduced & found in 19patients (63.33 %) In Group B Before treatment Avipaka was found in 29 patients(96.66 %) while After treatment Avipaka is found in 30 patients(100 %)02. In Group A Before treatment Tikta Amlodgara was found in 17patients (56.66%) but After treatment it reduced & found in 5patients (16.66 %) In Group B Before treatment Tikta Amlodgara was found in 24patients (80.00%) but After treatment it reduced & found in 21patients (70 %) 120   
  • 03. In Group A Before treatment Hrud Kanta Daha was found in 28patients (98.33%) while After treatment it reduced in 16 patients(53.33 %) In Group B Before treatment Hrud Kanta Daha was found in25 patients (83.33%) while After treatment it reduced in 28patients (93.33 %)04. In Group A Before treatment Chardi was found in 16 patients(53.33%) while After treatment it reduced in 8 patients (26.66 %) In Group B Before treatment Chardi was found in 14 patients(46.66%) while After treatment it reduced in 11 patients (36.66 %)05. In Group A Before treatment Shirshula was found in 17 patients(56.66%) while After treatment it reduced in 9 patients (30 %) In Group B Before treatment Shirshula was found in 27patients (90%) while After treatment it reduced in 27 patients(90%)Table No. 23Objective Criteria wise Group A Group B Criteria BT AT BT ATMean Free 22.23 19.52 20.28 20.1HCLMean Total 32.55 30.83 32.27 32.06Acid01. In Group A Before treatment Mean Free HCL was found in 22.23while After treatment it reduced in 19.52 121   
  • In Group B Before treatment Mean Free HCL was found in20.28 while After treatment it reduced in 20.1.02. In Group A Before treatment Mean Total Acid was found in32.55 while After treatment it reduced in 30.83 In Group B Before treatment Mean Total Acid was found in32.27 while After treatment it reduced in 32.06 122   
  • No.of Patients Graph No.1 : Distribution of Patients according to AgeNo.of Patients Graph No.2 : Distribution of Patients according to SexNo.of Patients Graph No. 3 : Distribution of Patients according to Religion. 123   
  • No.of Patients Graph No. 4 : Distribution of Patients according to Marital Status.No.of Patients Graph No. 5 : Distribution of Patients according to Educational Status.No.of Patients Graph No. 6 : Distribution of Patients according to Occupation. 124   
  • No.of Patients Graph No. 7 : Distribution of Patients according to Diet.No.of Patients Graph No. 8 : Distribution of Patients according to Prakruti.No.of Patients Graph No.9 : Distribution of Patients according to Vyasana. 125   
  • No.of Patients Graph No.10 : Distribution of Patients according to Economical Status.No.of Patients Graph No.11 : Distribution of Patients according to Agni.No.of Patients Graph No.12 : Distribution of Patients according to Koshta. 126   
  • No.of Patients Graph No.13 : Distribution of Patients according to Satva.No.of Patients Graph No.14 : Distribution of Patients according to Satmya.No.of Patients Graph No.15 : Distribution of Patients according to Sarata. 127   
  • No.of Patients Graph No.16 : Distribution of Patients according to Samhana.No.of Patients Graph No.17 : Distribution of Patients according to Dominance of Rasa.No.of Patients Graph No.18 : Distribution of Patients according to Type of Amlapitta. 128   
  • No.of Patients Graph No.19 : Distribution of Patients according to Manas Bhava.No.of Patients Graph No.20 : Distribution of Patients according to Abhyaran Shakti.No.of Patients Graph No.20 B : Distribution of Patients according to Jarana Shakti 129   
  • No.of Patients Graph No.21 : Distribution of Patients according to Sleeping Pattern.No.of Patients Graph No.22 : Distribution of Patients according to subjective criteria.No.of Patients Graph No.23 : Distribution of Patients according to objective criteria. 130   
  • RESULTSEffect of therapies: Total 60 patients were registered for treatment all 60 patientswere completed the course of whole treatment, 30 patients inGroup A, 30 patients in Group B. effect of Therapies on treated 60patients and the results of 60 being present here.Table No. 24Avipaka: Mean X Group S.D. S.E. t P BT ATGroup A 1.87 0.77 1.10 0.75 0.14 8.07 P<0.01Group B 2.23 2.2 0.033 0.56 0.1 0.33 P>0.01 The above chart shows that in group A, mean value ofAvipaka, before treatment was 1.87 which reduced to 0.77. Thereduction occurred is statistically significant which meansDrakshyadi Gutika is effective for Avipaka. While in Group B, the mean value of Avipaka,beforetreatment was 2.23 which reduced to 2.1 after treatment.The reduction occurred is statiscally not significan showing placebois not effective. 131   
  • Table No.25Tikta- Amlodgara. Mean X Group S.D. S.E. t P BT ATGroup A 0.77 0.17 0.6 0.6 0.11 5.45 P<0.01Group B 1.17 1.07 0.01 0.55 0.1 1 P>0.01 The above chart shows that in group A, mean value of Tikta-Amlodgara, before treatment was 0.77 which reduced to 0.17. Thereduction occurred is statistically significant which meansDrakshyadi Gutika is effective for Tikta- Amlodgara. While in Group B, the mean value of Tikta- Amlodgara,before treatment was 1.17 which reduced to 1.07 after treatment.The reduction occurred is statistically not significant showingplacebo is not effective.Table No. 26.Hrud Kantha Daha: Mean X S.D. S.E. t P Group BT ATGroup A 1.5 0.6 0.9 0.8 0.15 6 P<0.01Group B 1.83 1.77 0.067 0.64 0.12 0.56 P>0.01 The above chart shows that in group A, mean value of HrudKantha Daha, before treatment was 1.5 which reduced to 0.6. Thereduction occurred is statistically significant which meansDrakshyadi Gutika is effective for Hrud Kantha Daha. 132   
  • While in Group B, the mean value of Hrud Kantha Daha,before treatment was 1.833 which reduced to 1.77 after treatment.The reduction occurred is statistically not significant showingplacebo is not effective.Table No. 27.Chardi Mean X Group S.D. S.E. t P BT ATGroup A 0.87 0.27 0.6 0.72 0.13 4.61 P<0.01Group B 0.7 0.57 0.13 0.43 0.08 0.63 P>0.01 The above chart shows that in group A, mean value ofChardi, before treatment was 0.87 which reduced to 0.27. Thereduction occurred is statistically significant which meansDrakshyadi Gutika is effective for Chardi. While in Group B, the mean value of Chardi, beforetreatment was 0.7 which reduced to 0.57 after treatment. Thereduction occurred is statistically not significant showing placebo isnot effective.Table No. 28Shirashula: Group Mean S.D. S.E. t P BT AT XGroup A 0.9 0.3 0.6 0.72 0.13 4.61 P<0.01Group B 1.3 1.233 0.067 0.69 0.13 0.52 P>0.01 The above chart shows that in group A, mean value ofShirashula, before treatment was 0.9 which reduced to 0.3. The 133   
  • reduction occurred is statistically significant which meansDrakshyadi Gutika is effective for Shirashula. While in Group B, the mean value of Shirashula, beforetreatment was 1.3 which reduced to 1.233 after treatment. Thereduction occurred is statistically not significant showing placebo isnot effective.Table No. 29Free HCL Mean X Group S.D. S.E. t P BT ATGroup A 22.23 19.52 2.71 1.92 0.35 7.77 P<0.01Group B 20.28 20.1 0.15 1.33 0.23 0.63 P>0.01 The above chart shows that in group A, mean value of FreeHCL, before treatment was 22.23 which reduced to 19.52. Thereduction occurred is statistically significant which meansDrakshyadi Gutika is effective for Free HCL. While in Group B, the mean value of Free HCL, beforetreatment was 20.28 which reduced to 20.1 after treatment. Thereduction occurred is statistically not significant showing placebo isnot effective.Table No. 30Total Acid Mean X Group S.D. S.E. t P BT ATGroup A 32.55 30.83 1.72 1.04 0.19 9.05 P<0.01Group B 32.27 32.06 0.18 0.59 0.11 1.64 P>0.01 134   
  • The above chart shows that in group A, mean value of TotalAcid, before treatment was 32.55 which reduced to 30.83. Thereduction occurred is statistically significant which meansDrakshyadi Gutika is effective for Total Acid. While in Group B, the mean value of Total Acid, beforetreatment was 32.27 which reduced to 32.06 after treatment. Thereduction occurred is statistically not significant showing placebo isnot effective.Overall effect of Drakshyadi Gutika on 30 paitents ofAmlapitta Result Group A Group B No. of % No. of % patients patientsCured 12 40 0 0Improve 15 50 0 0Unchange 3 10 30 100 2 (Chi-Square Value) = 37.02 P<0.01 The above chart reveals that – In group A, out of 30 patients (40 %) were cured, 15 patients(50 %) were improved,while 3 patients (10 %) showed unchangeresult. In group B, out of 30 patients neither a single patient curednor improved. All 30 patients showed unchanged result. It means Drakshyadi Gutika is highly effective remedy forAmlapitta. The chi-Square Value of above table is 37.02 which is highlysignificant showing Drakshyadi Gutika, is highly effective inAmlapitta. 135   
  • DISCUSSION Ayurvedic stand apart from the rest of medical fraternity withits holistic approach to a patient as a conglomeration of mind, bodyand spirit too. The first and foremost task in Ayurvedic diseasemanagement is a proper understanding and description of itsetiopathogenesis. Acharya Vagbhata109 as well as AcharyaCharaka110 has clearly defined the role of Agni in theetiopathogenesis of disease. In recent years there has been anunprecedented increase of incidences related to GI system, due tochanges in life style, diet pattern, behavioural pattern etc,whichhamper the normal physiology of digestion/ Agni of body. Amlapitta is a disease of Annavaha Srotas i.e. AmasahaSamuttha which is mainly the seat for Agni. Any disturbance to Agnicaused due to irregular diet and behavioural pattern well as theinvolvement of mental stress and strain, leads to the diseaseAmlapitta. In Samhita some words have also been mentioned in thereference of Amlapitta. i.e. Jaratapitta seems as synonym forAmlapitta. and Amlaka, Dhumaka, Vidaha, Amlika, Prameelaka,Pitta Visuchika, Pittamala and Suktata, denotes the different aspectsof the abnormal state of Pitta. These are the major symptoms ofdyspeptic disease indicates towards Pittolvana condition. Charaka Samhita is the first medical literature bears 9 placesreference regarding Amlapitta have been found. Though he has notmentioned, Amlapitta as a separate disease entity, but from thereferences. It gives a clear cut indication regarding the Nidanas,Samprapti, and management in his period. 136   
  • Sushruta and Vagbhata have not at all mentioned the wordAmlapitta. Kashyap was the first person who described the diseasevividly and analyzed it on Doshik basis and give the importance ofits management. Madhavakara has described the diseaseseparately. Shrikanthadatta describes the disease by givingdifferent quotation. Latter workers of Sangrahakala followed thesame as Madhavakara and Kashyap.Nidana: Kashyap and Madhavakara both have given the long listof Nidanas of Amlapitta. They have different opinion regardingetiopathological factors. Kashyap has mentioned the Nidanas which represents theinvolvement of Doshas (Vatadayh) i.e. Tridoshs. Where asMadhavakara has mainly given Pitta aggravation factors responsiblefor this. Manasika factors also have strong role in the Nidanas ofAmlapitta, as stated in Charaka111 that Ama production is also dueto the involvement of mental stress and strain which hamper thenormal digestion and metabolism. In present day situation it hasbeen proved beyond doubt that the Manasika Bhavas have theirdirect impact on digestion and metabolism. Hence Manasika Bhavasshould be included in list of Amlapitta. Shadavidha Aharabhava are very important in explaining thephysiology of digestion and pathology caused by Nidanas. These sixfactors also greatly depend upon Ashtavidha Ahara Ayatana andDwadasasana Pravicharana. If looking according to Dosha functionsUshna is depend upon Pitta, Vayu and Kala and Vata, Kleda andSneha on Kapha. So any disturbance in the diet qualities or processmay start the pathogenesis by disturbing the digestion processdirectly (Agnidushti). 137   
  • In modern medicine, H. pylori takes a major role in theproduction of disease Amlapitta.Samprapti: The pathogenesis of the diseases as per Ayurvedic conceptrequires the three components i.e. Dosha, Dushya and Nidana. InAmlapitta the Nidanas are predominantly from the non complianceof dietetic code of selection and eating. However psychologicalstatus of a person plays an important role. While describing the Samprapti of Grahani Dosha AcharyaCharaka has mentioned the production of Amlapitta. According tohim when diet is improperly digested, it gets fermented and formsAmavisha, when this Amavisha gets mixed with Pitta, it developsthe disease Amlapitta. Where as Kashyap believed that the diseasecaused by vitiation of Doshas (Vatadaya) i.e. Tridosha causingMandagni leads to Vidagdhajirna manifesting as Amlapitta. Madhavakara in the line of Charaka describes thedevelopment of Amlapitta due to Pitta aggravating factors. AlsoKashyap considered Apakva Madya and Dugdha as causativefactors112 for the same and Acharya Charaka lists Dugdha as one ofthe Pathya for Amlapitta. Depending on the status of Nidanas either Kapha, Pitta orVata, the basic Samprapti of Amlapitta can be conceived from theclues given by Charaka113, Kashyap, Madhavakara and alsoSamprapti of Parinamashula describe by Madhavakara andVijayarakshita. Considering all Samprapties it can be conceived thatdisease Amlapitta can occur by all the three Doshas. The mainconsideration of the qualities concerned are Ushna, Tikshna, Katu, 138   
  • Amla and Sara Guna of Pitta, Guru, Shita, Manda Guna of Kaphaand Chala, Ruksha Guna of Vata. So, Amlapitta is a condition where Amla Guna is increaseddue to Samata causing Vataadi condition. Looking to the status of chief Dosha at the site of Amlapittai.e. Pitta, most common route is the Pitta predominant which havebeen consider by Charaka and subsequently by Madhavakara.However second common route of Amlapitta, pathogenesis is Kaphapredominant which have been consider by Kashyap and furthersupported by Vijayarakshita, while explaining the pathogenesis ofParinamashula. While explaining the pathogenesis of Amlapitta concept ofvarious Avaranas as explained by Charaka in Vatavyadhi should alsobe taken into account. It may be Kaphapittavrita Vata. HoweverAvarana may be three types.1. Samavata Avrita by Vriddhapitta and or Kapha2. Vriddhavata Avrita by Samapitta and or Kapha3. Vriddhavata Avrita by Vriddhapitta and or Kapha In the disease Amlapitta third pathogenesis is rare. Hencefirst two commonly encounter, which may give the clinicalconditions like Kapholvana and Pittolvana type of Amlapitta. As Chakrapani explains that Urdhva Amashaya is the seat forKapha and Adhoamashaya is the seat for Pitta. And also there ismore chance of involvement of local factor in the pathogenesisprocess. Hence Kapha and Pitta predominance should beconsidered. 139   
  • Also Acharya Charaka has given various conditions which mayhelp in explaining the pathogenesis of Amlapitta. These arePittavritta Vata114, Pittavrita Prana115, Kaphavrita Prana116 andPittavrita Samana116. The Samprapti of Gastro intestinal disorder constitutes thedifferent stages and each stage has been accepted as a separatedisease entity. Later on by various workers like Ajirna, Amlapitta,Parinama Shula etc. Vidagdhajirna is the initial stage of Amlapittacaused by vitiation of Pitta mainly Drava and Amlaguna. Vidagdhajirna is an acute and aetiology dependentdisorders, where as Amlapitta is a chronic disorder and oncemanifested then not dependent on Nidana. Vidagdhajirna isprecursor of Amlapitta and can be cured by Nidana Parivarjana onlyor with addition of Langhana and this is the main differencebetween two. Due to the similarities in Sthanika Doshas and Adhisthanadiseases like Vidagdhajirna Paittika Grahani, Paittika Atisara,Paittika Shula, Ammadrava Shula and Parinama Shula bears similarsymptomatologies and creates much confusion in diagnosis. Acarefully recorded history and Pratyatma ling of diseases maywaved out the suspicion in diagnosis. Because of the above description resembles with Amlapitta,great emphasis is given to disease by the research workers onAyurvedic medicine. All the later workers trying to correlatedAmlapitta with some modern disease entities such as gastritis,Peptic ulcer, duodenal ulcer, hyper acidity, hyperchlorhydira andalso hypochlorhydria. Probably to confirm to one characteristic ofthe entity namely its Bhishakamohakaratva or confusing nature. 140   
  • Many Researchers have brought out a new concept that Amlapitta isnot only hyperchlorhydria but the patients having both hyper as wellas hypochlorhydriya shows the same sign and symptoms ofAmlapitta. And they have concluded that Amlapitta is nothing butgastritis syndrome. Their results were very encouraging and taken anew approach towards the whole problem and thrown much light forfuture research workers. So, Gastritis refers to inflammation of the gastric mucosa,which is not a single disease but rather a group of disorder, due tointake of various irritant substances or endocrinal factors, due toany reflexes or due to any bacterial, viral or fungal infection out ofthese infection, H pylori is the most common ailments in thepathogenesis of Gastritis.Purvarupa: Purvarupa of disease is not mentioned in any classics.But according to Shadvidhakriyakala, the stage of Sanchaya andPrakopa may be considered as Purvarupa of disease.Rupa: Madhavakara has given general symptoms of Amlapitta asAvipaka, Klama, Utklesha, Tikta– Amla Udgara, Gaurava, Hrit–Kantha Daha, Aruchi etc. Madhavakara has classified Amlapitta intwo types according to gati i.e. Urdhvaga and Adhoga AmlapittaAdhoga variety cannot be diagnosed easily as mentioned byVangasena. It’s told that – there is very difficult to do differentialdiagnosis between Adhoga Amlapitta, Paittika Grahani and PaittikaAtisara. Also he told that even the intelligent Vaidyas get very muchconfused in clinical diagnosis and treatment. Hence it should be done according to Paittika Grahani.Madhavakar has also called it as Bhishak Mohakara disease117.Madhavakara has also mentioned 4 more types of Amlapitta. i.e. 141   
  • Vatika, Vata Kaphaja, Kaphaja and Kapha Pittaja. Kashyap hasmentioned 3 types i.e. Vatolvana, Pittolvana and Kapholvana.Urdhvaga variety of Amlapitta may be further classified as Doshikapredominant type. Acharya Kashyap explained about Upashaya and Anupashayaaccording to Doshik types. Amlapitta is considered as Sukhasadhyain earlier stage and of short duration but later on becomes KrichhraSadhya, Yapya and becomes Asadhya when accompanied withUpadravas. Upadravas has not been described by any ancientAcharya except Kashyap and Gananatha Sen i.e. Jwara, Atisara,Pandu etc. Acharya Kashyap and Charaka have mentioned that thisdisease occurs mostly to the persons having Jihvalaulya. Henceafter some recovery the person again gets involved in Mithya AharaVihara due to Jihvalaulya and the disease again gets provoked. Thisvicious cycle goes on and the disease becomes chronic. Acharyashave described various guideline principles for the management. Among them, Nidana Parivarjana plays major role. Variouspreventive measures are explained which helps in preventing aswell as development of Amlapitta. Treatment modality mainlyincludes Shodhana and Shamana therapy. Among Shodhana,Vamana and Virechana have been advised followed by Basti. InShamana therapy, Madhura, Tikta, Katu, Amla predominant RasaSheeta, Ushna Virya drugs have been used. So, in the present study‘Drakshyadi Gutika’ has been given patients having pittapredominant Amlapitta, as it contains drugs having Madhura SheetaVirya and Guru, Snigdha property. Amlapitta as its maximum drugs are having Katurasa, Laghu,Ruksha property and Ushna Virya. 142   
  • Also Pathya-Aathya forms an important part of the treatmentin this disease. Patient has been advised to follow Dwadasha asanaPravicharana and restrict the use of Amla, Lavana, Katu Rasa,Ushna and Tikshna Guna diet according to their Doshikapredominance. With an aims and objective to provide a better diagnostic andtherapeutic approach this study had been conducted. Patientscoming to our department O.P.D. or the diagnosed cases ofAmlapitta were properly examined on the basis of speciallyprepared protocol and data recorded from the study are as followsAge :- Maximum no. of patients, i.e. 35 patients (58.33 %) werebelonging to 20-30 yrs. Age group followed by 14 patients (23.33%) in 31-40 yr. this indicates that the middle aged populations areaffected by this disease more, which is pitta predominant period oflife. This pitta predominance makes disease chronic and krichhrasadhya. Further this age group are one for whom hurry, worry & curryhas been advised to be restricted. In this age group nobody is goingto restrict themselves for any dietetic and behavioural code. Thesedecades are most productive age of the human, hence everybody isunder stress to deliver more within short period.Sex :- Out of 60 patients; 36 patients (60 %) were male. This maybe due to faulty dietary habits, increased stress & strain amongmales & also due to habits like smoking pan etc. 143   
  • Religion :- Maximum 41 patients (81.66 %) patients were Hindu. Thehospital where study have been conducted is situated in Hindupredominant area and most of the population coming to the hospitalbelong to same community. So, it can not be concluded that Hinduare more prone to Amlapitta.Marital status :- Maximum i.e. 45 patients (75 %) patients were married,because this status is related to middle age group. Also familyinvolved patients were under stress due to various reasons.Educational status :- In this study 23 patients (38.33 %) were educated this maybe because of fast life style, irregular food habits stressful conditionthese reasons for the incidence of Amla pitta.Occupations :- 21 patients (35 %) were service holder followed by 14patients (23.33 %) were housewives. This incidence in serviceholder, may be due to hurried & worried life irregular diet habits.Etc. where as in housewives, may be under stress due to variousfamiliar reasons.Diet :- Maximum no. of patients i.e. 38 patients (63.33 %) weremixed diet the reason may be excessive use of spicy food whichprovak the pitta-kapha dosha presominantly.Deha prakriti :- Maximum 51.66 % (31 patients) were having vatta-pittaprakriti while 26.66 % (16 patients) had vatta kapha prakriti. 144   
  • Vyasana :- Maximum patients i.e. 17 patients (28.33 %) were used totea while 25 % (15 patients) were addicted to alcohol. So this may impair Agni & favour for manifestation ofAmlapitta.Social Economical status :- 27 patients (45 %) were from middle class & reason for thismay be untimely food intake increase family members in acongested area or more prone to stress & strain in their routine life.Agni :-In present study maximum patients are of mandagni (40 patients)(66.66 %) these type of Agni’s causes Agnimandya which is theroot cause of Urdhwaga Amlapitta.Koshtha :- It is observed that Urdhwaga Amlapitta occurs is more in thepeople having madhyama koshtha followed by Mrudu kostha.Madhyama & Mrudu koshtha reflect the predominance of kapha &pitta which are the main dosha involved in pathogenesis ofUrdhwaga Amlapitta.Satva, Satmya, Sarata, Samhanana :-27 patients (45 %) were having Madhyam Satva.32 patients (53.33 %) were having Madhyam Satmya.43 patients (71.67 %) were having Madhyam Sarata.40 patients (66.66 %) were having Madhyam Samhanana.This reflects the general Sara, Satva, Samhanana, in the society &this can not be correlated to disease. 145   
  • Dominance of Rasa :- Maximum no. of patients 21 patients (35 %) were taking katurasa pradhana diet followed by 11 patients (18.33 %) were takingAmla rasa pradhana diet excessive intake of these Rasas vitiatesPitta & kapha which finally may lead to Amlapitta.Ahara Shakti :- 33 patients (55%) were having avara Abhyavaharana Shaktifollowed by 22 patients (36.66%) Madhyama AbhyavaharanaShakti. 36 patients (60%) were having Madhyam Jarana Shaktifollowed by 21 patients (35%) were having Avara Jarana Shakti.The resion probably for this is, in this disease there is impairment ofAgni.Sleeping habit :- Majority of the patients were (65 %) having Samyaka Nidrafollowed by (11.66 %) having Alpa Nidra. This may be due to pain and burning sensation in chest &abdomen.Manasa Bhava:- Majority of the patients wre 61.66% having Chinta followedby 43.33% having Krodha which is responsible for improperdigestion leads to Ajirna like condition as mentioned in Ayurvedicclassics. 146   
  • Cordinal signs & Symptoms As mentioned earlier in theclinical study, Avipaka was found in98.33% Hrudkhanta Daha in 88.33%, Shirshula in 73.33% Tiktaamlodagara in 68.33% & Chardi 50%. As these were the cardinalsymptoms. It was expected to haved finding like this but thequantum of these findings was important these findings may be dueto Amla/ Katu Pradhana Rasa diet or other faulty dietetic habitsmental condition sleeping pattern etc. the degree of Severity wasdifferent in each & every patients.Total effect of therapy In group A, out of 30 patients (40 %) were cured, 15 patients(50 %) were improved,while 3 patients (10 %) showed unchangeresult. In group B, out of 30 patients neither a single patient curednor improved. All 30 patients showed unchanged result. It means Drakshyadi Gutika is highly effective remedy forAmlapitta. The chi-Square Value is 37.02 which is highly significantshowing Drakshyadi Gutika, is highly effective in Amlapitta. 147   
  • SUMMARY The Dissertation entitled “To study the efficacy ofDrakshyadi Gutika in Amlapitta.” Comprises :- 1. Introduction 2. Aims and objectives 3. Review of literature a. Historical view b. Ayurvedic view c. Modern view d. Drug review 4. Clinical study 5. Observation & Results 6. Discussion 7. Summary & Conclusion 8. References 9. Bibliography Introduction gives brief idea about Amlapitta & UrdhwagaAmlapitta, Aim & Objectives of the study. In the Historical review, reference regarding the Amlapittadiseases during different period of time viz. vedic period, samhitakala were compied under the heading Historical Review ofAmlapitta. Amla pitta – Ayurvedic view of which deals with Ayurvedicconcept of the diseases. Viz. Etymology Defination, Synonyms,Classification, Aetiology, pathogenesis, premonitory, Symptom, 148   
  • Symptoms Exploratory, Symptoms, Complications, Prognosis,Differential Diagnosis, Treatment, Pathya-Apathya. Amlapitta – Modern review, the description of Amlapitta frommodern point of view as Gastritis was presented c Anatomy &Physiology of Stomach, definition, actiology, pathology, signs &Symptoms, management and at last Gastric Analysis Test & test ofH. pylori antibody defection has been described. Drug Review describes the Research drugs c their ingredients& method of preparations.Clinical study deals with the details of present study vir. Moterical &Methods, Inclusion Criteria, Exclusion Criteria, Researchmethodology, controlled conditions & lastly criteria for assessmentof resuls.Observations & Results – observation were made c regard to age,sex etc. the results of the study were analyzed statistically and arepresented with discussion.It also includes discussion about probable mode of action ofresearch drugs on Amlapitta.Summary of contents of this dissertation have been mentioned.Clonclusion drawn on the basis of present study have beendiscussed and lastly references & Bibliography is includedrespectively. 149   
  • CONCLUSIONS In Brihattrayi Amlapitta has not been considered as a separate diseases entity Kashyapa & Madhavakara have given a separate disease status to Amlapitta. Indugence of katu, ruksha, guruahar, vegvidharna indicates origin of the diseases. From this study it can be concluded that non compliance fo code of healthy diet select & eating plays a major role in causation of this disease. Hence we can say that code & conduct of healthy eating is important to achieve early & better result of the treatment as Nidaha parivarajana. Amlapitta is the burning problem in society due to changing in lifestyle. The mental irresistible stress & strain of this present era are related with the pathogenesis of this disease. Krodha, Chinta, Bhaya these manasika factors plays a major role as an aetiological factor. According to present knowledge the normal functioning of the Agni, Pachaka pitta means the secret enzymatic functioning of Gastro-intestinal tract is dearrange in this disease. Amlapitta is result of Agnidusti &it is chronic in nature and difficult to care Rasa and Rakta is involved as Dushya & Rasa, Rakta, Annavaha & Purishvaha strotas is involved. 150   
  •  Amlapitta is a Tridoshaja vyadhi with the mean outsprint dosha Pitta. Madhavakara in the lines of charaka has described the pitta predominant Amlapitta where as kashyapa has described kapha predominant Amlapitta. Vidagahajirna is a previous stage of the disease production as explained by charaka. Study of etiopathogenesis clearly indicates the predominance either kapha or pitta in initiation of Amlapitta pathogenesis. Sometimes improper assessment of prakriti, and wrong diagnosis also plays a major role in the production of disease. Drug having the properties like deepen pachana & balya are useful in the treatment of Amlapitta. The drug under trial “Drakshyadi Gutika” was effective in hyperacidity condition this beneficial effect of trial drug may be due to madhura rasa, laghu Ruksha property & Vata- Pitta hara action of the combined drug of this preperation. In Drakshyadi Gutika group, better results were obtained as compared to placebo. It may be variation In dosage of both drugs. It is recommended that the study should carry out in large no. of patients to evaluate & analyze the results Objective paramete & higher investigations should be incorporated in the study. As Amlapitta disease may be a chronic disease follow up should be kept for longer duration and strictly pathya apathy compliance is required for the cure of disease. 151   
  • ABBREVIATIONSA. H. Ashtanga HridayaA. S. Ashtanga SangrahaB. P. BhavaprakashaBh. Bhela samhitaCh. Charaka samhitaCh. Su. Chark SutrasthanaCh. Chi. Charak ChikitsasthanaChakra. ChakrapaniHa. Sam. Harita samihitaKa. Kashyapa smahitaKa. Sam. Kashyapa samhitaM. N. Madhava NidanaNi. NidansthanaPu. Purva KhandaSha. SharangadharaSi. Siddhi sthanaSu. Sushruta samhitaUp. UttartantraVi. VimanasthanaY. R. Yogaratnakara.S.N. Siddhant NidanaKs. Khi. Kashyap Khilsthana 152   
  • REFERENCESIntroduction :1. Ka.Khi. 7/12 5. Ka.Khi. 16/12. Ch.Chi. 15/3/4 6. M.Ni. 12/13. Ch.Chi. 15/44-49 7. API Medicine 7th Edition P.No.5634. As.Hr.Ni. 12/1Conceptual Study :8. Ch.Chi. 15/3 20. Cha.Chi.15/42-449. Ch.Chi. 15/3 21. Ma.Ni. 51/210. Ch.Chi.15/15 22. Ch.Chi.15/911. Ch.Chi. 15/13 23. Ah.Su. 9/2012. Ch.Chi.15/15 24. Su.Su. 21/13, Ah.Su. 12/1713. Ch.Chi. 15/42 25. Cha.Chi.15/614. Ch.Chi.15/13 26. Cha.Chi. 15/615. Ch.Chi. 15/15 27. Cha.Chi.15/1016. Ch.Chi.15/13 28. Cha.Chi. 5/1117. Ch.Chi.15/13 29. Cha.Chi.15/1118. Ch.Chi.15/13 30. Cha.Cha.6/1419. Ch.Chi. 15/15 31. Su.Su. 21/932. Su.Su.25/27-28 34. Su.Su. 46/487-48833. Su.Su. 21/16Disease Review :35. Ch.Chi. 15/3 40. Ch.Su. 27/2536. Ch.Su. 20/14 41. Ch.Su. 7/14837. Cha.Su.25/40 42. Ch.Su. 12/5238. Ch.Su. 26/43 43. Ch.Chi. 15/4739. Ch.Su. 26/103 153   
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  • Delhi162