Drakshyadi gutika in amlapitta kc

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INTRODUCTION

Today’s life style is completely changed by all the means our

diet pattern, life styles and behavioral pattern is changed & it is not

suitable for our normal physiology of digestion of body & all above

mentioned causes aggravated dosha which creat agnimandya & due

to improperly it metabolized it get convert into shukata (vitiated

liquid acid) & this gets situated in Amahsaya which is called as

Amlapitta1.

In recent years there has been an unprecedented increase of

incidences related to GI system due to changing in life style. Diet

pattern, behavioral pattern & mental stress & strain.

Amlapitta is a such type of GI disorder due to same causative

factor as above described in Ayurvedic parlance, closely resembles

with Gastritis in modern science also and in chronic stage it may

lead to ulceration condition.

Charak & Kashyapa have clearly indicated that the Grahani

Dosha & Amlapitta occur in the persons who could not check the

temptation of food. Ajirna ofter encountering the specific Doshas &

affinity with specific site may cause various diseases. Annavisha

produces due to Ajirna when mixed with pittadi Dosha & lodges in

Amashaya then it produces the Amlapittadi diseases.

The first & foremost task in Ayurvedic disease management is

a proper understanding & description of its etiopathogenesis. In this

respect Acharya Charaka has told that Agni is responsible for Ayu,

Varna, Bala, Swasthya. Utsaha, Upachaya, Prabha, Ojo & Teja & it

also gives the importance as long life in the functioning state2 &

even death in unfunctioning state of Agni also Acharya Charaka3. &

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Acharya Vagbhata has clearly defined the role of Agni in the

etiopathogenesis of all the human ailments4.

Charak has explained the sequential progression of diseases

of G.I.T. to which Sanghara Granthakara has given a separate

disease status. In samhita Amlapitta is no mentioned as a separate

disease entity but there are several references in charaka samhita

regarding 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 of

the disease5. And analyzed first it only Doshik basis, where as

madhavakara gives status to the disease and he further classified it

on according to Gati i.e. Urdhvaga Amlapitta & Adhoga Amlapitta as

well as on Doshika basis6.

Acharya Kashapa belived that the disease is caused by

vitiation of Doshas (Tridosha) causing mandagni leading to

vidagdhajirna manifesting as Amlapitta.

Madhavakara following Charaka has described the

development of Amlapitta due to Vitiation of pitta which is already

increased due to its own causes. This disorder is the result of

Grahani Dosha.

Gastritis & non-ulcer dyspepsia have been co-related with

Amlapitta by several MD & Ph. D. Scholars of Ayurveda. As per

Modern interpretation the symptoms of Amlapitta found in certain

pathophysiological condition of GI such as hyperacidity with occur in

APD diseases7.

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Modern medicine is not having proper medication for gastric

dyspepsia. Ayurveda has a lot to offer in this regard. Ayurvedic

physicions are providing cure for the patients of these chronic

dyspeptic disorders.

Several single & compound drug has been tried in this

disease.

Acharyas told to use the drugs which are having Tikta-

Madhura rasa. Madhura Vipaka Sheeta Virya & Laghu Ruksha

property with kapha-Pittahara action.

Taking all these points into consideration the study was

planned to evaluate aims & objectives.

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AIM & OBJECTIVES

1. 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.

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BRIEF REVIEW OF ANNAVAHA SROTASA

ANATOMICAL & PHYSIOLOGICAL ASPECTS.

DEFINATION :-

The word Annavaha srotasa means the channel through which

food is transported. The functions of organs of ANNAVAHA SROTAS

(Alimentary system) concerned with ANNA ADANA (ingestion of

food), 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 to

sushruta - Amashaya & Annavahi Dhamanyas. Charaka has said

that Amashaya and vamparshva are the Moola of Annavaha srotasa.

Acharya Sushruta has said that Amashaya and Annavahi

Dhamanyas are the Moola of Annavaha srotasa. Chakapani has

given two terminologies - Urdhva and Adho for Amashya. Urdhva

Amashaya was the place of kapha while Adho Amashaya was the

palce of pitta. The deglutination and ingestion process of food is

start from mouth and in upper part of the stomach. main digestive

process is start from stomach. Digestive juices secreat from lower

part of the stomach and intestine Bile and panereatic juices secret

from liver and pancreas than after come into the small intestine.

Therefore we can include oesophagus and upper part of the

stomach in Urdhva Amashaya and lower part of the stomach &

small intestine in Adho Amashaya. The term Annavahi Dhamanyas

are also a Moola of Annavaha srotasa. It means the channels which

transplant the end products of Anna from the intestine to the

plasma blood. Under the microscope the mucous membrance of the

small intestine contains millions of finger like projections known as

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villia. This villus is lined by a single layer of epithelial cells and small

arteries, veins and lymphatic vessels. In function, the villi act as a

semi permeasble membrane and permit the passage of digested

food through the Rasavaha and Raktavaha srotansi contained in

their. In other words, these microscopic parts of the membrane

carry out the transportation of the Anna Rasa though the intestinal

barrier.

Pittadhara Kala:-

Acharya Sushruta & vagbhatta both have described pittadhara

kala. Acharya Sushruta say "THe sixth Kala situated between

Pakvashaya and Amashaya is the pittadhara kala and it is known as

Grahani. In his view, "The intrgity of Grahani depends upon Agni9."

In charak's opinion "Grahani is so called beacuse it receives and

retains the food for the duration of its digestion. He observed that

the food, which has reached the Amashaya after under going

digestion absorbed." Pittadhara kala is provides the digestive juices

collectively termed as Pachakagni or Jatharagni. These juices not

only digest the food but also aid the sepration of the sara from the

kittabhaga10. (Sara kitta vibhajana kriya) The description of

pittadhara Kala shows that it is a macroscopic structure which not

only 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 Agni

and responsible for the reception, digestion, separation and

propulsion of the food. The Samana Vayu function are similar to

intrinsic nervous system of the stomach and intestine. This system

is related to brain and spinal cord. The peristaltic movement of

intestine are responsible for mechanically breakdowns intestinal

contents and throughly mixed up with the juice of pancreas liver

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and intestine. They absorbed through the intestinal wall. This has

been described the function of Samana Vayu as digestion of food,

separation of nutrients fraction of food and expulsion of undigested

food. (Annapachana, Vivechana and Munchana.) So, as an

Anatomical view, we can consider fallowing orgens & systems in

Annavaha 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 the

small intestine and lower part of the stomach also.

(C) Annavali Dhamanyas:- The channels that receives the end

particlesof 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 in

the digestion of food Grahani is also considered as a pittadhara

kala. Avastha paka is the first phase and vipaka is the second

phase. Avasthapaka is the first phase of the digestion completed by

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Pachakagni in Annawaha srotasa, and vipaka is the second phase of

digestion that completed by Bhutagni and Dhatvagni. vipaka is start

after 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 Khadita

that reaches to Amashaya forms in to Madhura Bhava. At this stage

salivary digestion will be completed in the fundus of stomach, were

the insoluble starch and polysaccharides.

Converted in to soluble dextrin under the influence of salivary

amylase. The final Rasa in the upper portion of the urdhava

Amashaya is madhura. The prana vayu is responsible for the entire

movement of food from the mouth to Amashaya. The Bodhaka

Kapha and Kledaka Kapha is also responsible for Madhura

Avasthapaka. Bodhaka kapha is responsible for perception of taste

in the mouth. The Bodhaka Kapha is analogue of saliva which

dissolves some substances, the enzyme content begins to act and it

lubricates the food, kledaka kapha also lubricates the food in

Amashaya. We can considered it as mucine.

(ii) Amla Avasthapaka 14:-

Amla types of strava occurs here, and after completition of it.

Ahara becomes Amla. So it is called Amla Avasthapaka. In this

stage Ahara converting in to insoluble proteins to soluble proteins,

under the influence of the pepsin, in the presence of HCL. According

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to charaka and vagbhatta the final out come of the entire gastric

digestion is the acidified chyme, that is interpreted by ' Tikakar

chakapani as pakvapakva (partialy digested). At this phase the

ahara pachana is due to an amla factor sereted by the urdhva

Amashaya. The ahara which becomes Amla Bhava, passes in to the

next lower portion of Annavaha srotasa, were Achhapitta is

secreted. Modern science says that the acidified chyme passes down

from the pylorus in to the duodenum. acts as a stimulates the

duodeneal glands (Burner's gland) to secreate a number of internal

secretion like secretin, cholecystokinin, enterogastrone,

Pancreozymine etc. The presence of acid in duodenum is liberates

the circulation of secretin hormone and stimulate the flow of

pancreatic juice. Secretins also enhance the secretion of bile and

intestinal juice. The pancreozymine and intestinal hormone also

stimulates the secretions of enzymes from the pancreas, occurs in

intestinal mucosa cholecystokinin also responsible for the

contraction of the gallbladder and therefore discharges of bile in

duodenum. All these hormeones acts due to entering the acidified

chyme in to duodemum and there fore pancreatic juices, biles and

intestinal juices secreated in small intestine. In Ayuarveda,

Achhapitta is combination of these three juices. We can say that

madern physiology also supports the Ayurvedic approach of

Achhapitta Nirman Kriya. Due to these juices all the Facts and semi

digested proteins are completly digested and converted in to fatty

acids and glyceral and Amino acids.

(iii) Katu Avasthapaka15:-

In this stage, the materials phases down the pakvashaya from

the Amashya and being dried by Agni. and rendered in to lumps.

(paripindita pakva) During this process vayu and Mala are

produced. In Modern physiology, minerals from the end products of

digested food, the remaining materials are converted in to feaces.

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The bacteria precessed on it and created some vitamins and indole

and sketol like gases.

(B) VIPAKA:-

According to charaka the digestion of food by jatharagni break

down the food in to five physicochemical groups viz parthiva, Apya,

Agneya, Vayavya and Akashiya. Activated Agni Bhuta present in

each one of these Bhautika groups. The Bhutagni thus activated

digests the substance of that group16.

(i) Bhutagni Paka17 :-

Bhutagni paka follows jatharagni paka and it completes the

process of intestinal digestion. After Bhutagni paka, the Ahara Rasa

is completed and the Rasa shoshana is possible. Thus the Agni

constituents of the predominantly parthiva molecule spoken as

parthivagni digest the substances of the molecules. Similarly

Apyagnidi gets the substance of the moleoules of Apya and it for

Agneya, Vayavya, and Akashiya, the out come of this type of

digestion according to chakrapani is the transformation of the

charcteristic qualities of each group and the assumption by them of

vilakshana Gunas or all together new qualities.

(ii) Dhatvagni Paka18:-

After Jatharagni Paka & Bhutagni Paka of the Ahara Rasa is

created and it is absorbed from the Anna Vaha Srotasa and

circulates throughout the body by Dhamanies This Annarasa

undergoes the process of Dhatvagni Vyapara and thus saptadhatus

are created. Seven different kinds of Dhatvagnis correspondence to

specific seven types of Dhatus viz Rasagni, Raktagni, Mansagni,

Medogni, Asthyagni, Majjagni and Shukragni. The Rasagni does the

digestion of the Ahararasa so Rasadhatu and its Mala are

developed. In the same process every Dhatvagni digests the same

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molecular particles of Ahararasa and same Dhatus were developed.

Acharya Charaka said that the pakas act upon seven Dhatus giving

rise to Kitta and prasada bhaga19.

The prasada paka is related to anabolic aspects and the kitta

paka is of the catabolic. Dhatvagni converts the Ahara rasa in to

sthayi & Asthayi Dhatu. Prasada Paka is being an Asthayi Dhatu.

Asthayi Dhatu is converted into sthayi Dhatu by particular

Dhatvagni. In Dhatvagni Vyapara Kitta paka like sveda, Mutra,

Purisha, vata pitta, kapha smashru, Nakha, Kesha etc are also

developed.

Indian medicine books have given various concepts like

khalekapota Nyaya, Ksheeradadhi Nyaya. Kedari Kulya etc. on

Dhatvagni Vyapara or Dhatu Nirman.

PATHOPHYSIOLOGICAL ASPECTS OF ANNAVAHA SROTASA

Dusti 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. Ahita

bhojana means the food taken by the person is not reliable for Phis

health. Agni Dusti means the improper digestive power. First three

causative factors creat Agni Dusti by Dosha Vaishmya. Agni Dustri,

the fourth causes is due to some diseases like Rajayakshma. All of

above causative factors create the disease of Annavaha srotasa like

Amlapitta. They generate the Adadrasha & dusha vaisamya, which

responsible for the aggravation of the process of the diseases like

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Ajirna, Chhardi, Atisara, Arasha, Grahani, Amlapitta, Alasaka,

Aruchi, Visuchika etc. These causative factors vitiate the pittadhara

kala. So these symptoms are developed.

DUSTI LAKSHANA :-

Four main symptoms of the Annavaha srotodusti. They are the

cardinal 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 interesting

of food intake even though the food is very good and delicious.

Acharya sushruta said that Arochaka is a disease, which has

complete loss of interest in food due to shoka, Bhaya, Krodha,

Lobha etc. Vitiated vatadi doshas and manasika Bhavas that staying

in Jihva, Hridaya and Bhaktayana. According to sushruta, shokadi

Manasika Bhavas as the causative factors of it. They create vatadi

Dosha 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 kriya

is disturbed due to Agni vaishmya & avipaka is created. The Grahani

is the main organ in Annavaha srotasa as an anatamical and

physiological both. In annavaha srotodusti, Grahani Dosha is there.

So, the pittadhara kala and Agni is also distrubed, because there is

a reciprocal relationship between Agni & Grahani.

In the modern science, the mucosal membrane lined in the

stomach and small intestine is responsible for the secretion of

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enzymes. If there is some distrubance in it, the enzymes are not

secreted in proper way. In this condition the indigestion or Avipaka

is occurred.

Acute & chronic gastritis, peptic ulcer, tropical & nontropical

sprue, malabsorption, syndroimes, non ulcer dyspepsia. etc,

disease. have Avipaka as a first symptom In all these diseases inner

mucous membrance is affected which called pitadhara kala in

Ayurveda.

(3) Chhardi :-

Meaning of chhrdi is forceful expulsions of the gastric and / or

duodenal contents through the mouth. It is due to Avipaka and Agni

Vaishamya. Mainly vata Dosha – Udana and Samana Vayu

distrubed. It is occured when any part of the upper gastro

intestinal tract becomes excessively irrited Impulses are transmitted

by both vagal and sympathetic afferent to the bilateral vomitting

center of the Medulla, which lies near the tractus solitarious. Motor

impulses are tremsmitted though the 5th, 7th, 9th, 10th and 12th

cranial nerves to the upper gastro intestinal tract and through the

spinal nerves to the diapharm and abdominal muscles. This nervous

mechanism is considered as a vitiation of vata dosha in Ayurveda.

Mainly observation or anti peristalsis activity is responsible for

vomiting. Irritation of mucus membrance like gstritis, enteritis etc is

also responsible for it.

(4) Anannabhilasha :-

Anannabhilasha means the total loss of desirement or interest

of food even though it is given as per demand of the person.

Chakarapani has said that the pt. can digest the Ahara in to

stomach through the mouth but the loss of interest of food is there.

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In modern science, it is due to mental stress or sensation of stiety

while complete loss of appetitite is not there.

Digestive System

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CONCEPT OF DIGESTION

Gastro intestinal digestion or change in the state or form of

the food substances in Aamaashaya and Pakvaashaya in the course

of digestive process. Two phases of the Paaka i.e, Prapaaka and

Vipaaka have been envisaged. The Prapaka has been defined by

Chakrapanidatta as Prathama Paka22. These changes have been

described in terms of the Rasa or taste of the end products of

gastro-intestinal digestion viz. Madhura, Amla and Katu23. Prapaka

commences right from the time, when food is introduced into the

mouth. This aspect of digestion and the digestion in the upper

portion of Urdhwa Aamaashaya are comprehended by Madhura

Bhava. When the food is introduced into the mouth, the perception

of its Rasa takes place which is stated to be enabled by Bodhaka

Kapha24. The next event which takes place is Vibhajana of food by

the Tejas element of the Lala Strava, which is described in

Ayurveda Sootra and Yoganand Natha commentary. Taste

perception and preparatory digestion and the beginning of the

Madhura Bhava occurs here. The movements are brought by Prana

Vayu25. The second phase i.e. Amla Avasthaa Paaka involves the

Vidagdhavastha of food. The term Vidagdha has been interpreted by

Chakrapanidatta as 'Pakva- Aapakvam' or 'Kinchit Pakvam Kinchit

Aapkvam' i.e. partly or not fully digested26. As the partly digested

food which has attained Amla Bhaava is moved down, Achha Pitta is

secreted27.

The term amla refers to the production of Pitta under

influence of the Aahaara which has since assumed Amla Bhaava.

The third aspect of Avasthaa Paaka is the Katu Bhava. This aspect

relates to the acrid and pungent nature of the reactions that occur

in the Pakvaashaya. Charaka says that the material passed down

from the Aamaashaya having reached the Pakvaashaya is

dehydrated and converted into lumps by heat28.

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Chakrapanidatta has observed that the term Shoshana used

by Charaka instead of Paachana is significant. The former relates to

the dehydration of the food residue which has been brought to

Pakvaashaya whereas the later refers to the digestion of food in the

Aamaashaya by Agni. The term 'Paripindita Pakvasya' according to

him refers to the process of formation of fecal lumps. The term

'Vaayu syat KatubhaVaatah' describes the production of acrid and

pungent gas29. Pakvaashaya is the seat of Vayu where five Vayus

are produced.

According to Sushruta, the separation of Rasa, Mala and

Mootra brought about by Paachaka Pitta. Sharangdhara and

Bhaavamishra have stated that the Saara Bhaaga is known as Rasa,

and the Saraheena Bhaaga is Mala. The factors responsible for

digestion is six Ahara Parinama Kara Bhavas30. i.e.

i) Ushma ii) Vayu iii) Kleda

iv) sneha v) Kala and vi) Samyoga.

i) Ushma: Ushma is a quality of Agni mahabhuta only. In this

regard two terms are to be considered i.e. Agni and Pitta. Sushruta

explains that there is no Agni excepts Pitta in body31. Out of five

types of Pitta, Pachaka Pitta situated in Amashaya performs all

favorable and unfavorable functions described as functions of Agni

various secretion of GIT can be considered in the light of Pachaka

Pitta. So release of these secretions in proper time, quality including

the temperature of stomach is essential for proper digestion,

disturbance of any will lead to Agni Dusti and start the Samprapti of

disease.

ii) Vayu: Samana Vayu is seated in Amashaya and helps the

Pachaka Pitta in digestion. According to Sushruta31. There is vicious

relationship between Prana - Apana – Samana Vayu. Where as

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Prana and Apana Vayu helps to maintain the Agni. Prana Vayu

directly takes place in act of digestion by transporting food upto

stomach and Samana Vayu moves in koshtha all around and

performs the functions attributed to Agni, Grahani and Pachaka

Pitta. Three phases of gastric acid secretion can be considered

under the karma of Vayu. That is cephalic phase, gastric phase and

intestinal phase. The apakarshana, grahana and munchana karma

of Vayu are essential for proper digestion. Any exacerbate or

cessation in these functions will lead to improper digestion. As

certain time is required for proper digestion, delayed emptying will

cause the shuktapaka and formation of annavisha, which are the

essential features of Grahani dosha samprapti. Now, it is clear that

all 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. The

etiological factors like Krodha, Shoka, Bhaya, Chinta and other

stress factor work through the vagus chain, which is mediating

through Vayu. Provocation of Vata by any factor will result in hyper

secretion leading to hyperactivity.

iii) Kleda: This factor is necessary for proper digestion. Kleda looses

and emulsifies the food substance. So that it may easily digested33.

This function is performed mainly liquid portion of food. Kledaka and

Bodhaka Kapha may be considered in this regard. Charaka has

mentioned the function of disintegration and softening of food

substance in the Koshtha due to ‘Drava’ and ‘Sneha’. Though Kapha

has not been mentioned having Drava quality but Kapha is made up

of ‘Ap’ dhatu and so that Kapha most possess Dravata but it

depends upon the temp. so the function of Kledaka Kapha can be

summarized as Kledana - Shithilikarana – Mridukarana and

Samghata Bheda. Also the functioning of Bodhaka Kapha may

include moistening of mouth to help in speech and helps in

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mastication. Dravata is also the quality of Pitta and Kledana function

can also be attributed to the dravansha of Pachaka Pitta. The

excessive klinnata may hamper the Agni directly as mentioned in

the literature that Dravata create the Agni. Ingestion of any

Atiushna, Tikshna and Katu Dravya may cause excessive secretion

of mucosa, which may interfare with digestion process and cause

the Vidagdha Avastha in excess leading to Ajirna etc. in the same

way increase in Kapha cause Mandhaagni. Hence, if the function of

Kapha create, the ulcer can directly be produced due to action of

Agni on mucosa. Hence, a very delicate balance of responsible

factor is required for proper digestion.

iv) Sneha: Sneha mainly comes from Ahara, Kapha also have the

property of Sneha. Also Chakrapani clarifies that sneha is present in

feeble quantities in Pitta. Hence it can be said that sneha is also

quality of kledaka Kapha and Pachaka Pitta. Sneha performs the

function of Mardava of food stuff. Ultimately it helps in the proper

mastication and churning by stomach musculature, so that proper

digestion can takes place. The decrease in the quality of Sneha may

damage the intestinal mucosa due to roughness of food stuff and

also due to Ruksha Guna of various food materials. Hence,

Snehaguna also performs the protective effect to the stomach

musculature. Decrease of Sneha in stomach will lead to provocation

of Vayu (Samana Vayu) which causes imbalance of Agni leading to

Agni Vaishamya.

v) Kala: Kala means mainly the time required for the digestion of

ingested food stuff. Time required for the proper secretion of all the

digestive factors and for proper digestion and absorption. But other

time consideration are also necessary for proper digestion and

absorption of food i.e. Kshudhakala (hunger time). Trishnakala,

Doshakala and also Charvana Kala. The meals taken without proper

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digestion of previous meal is called adhyasana and this untimely,

food intake causes Amadosha which leads to Agnidushti. Emptying

of 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 Munchana

period leading to improper digestion and absorption, which will lead

further provocation of Doshas and Agni Dushti.

vi) Samyoga: Equilibrium of all the above factor is necessary for

the proper digestion of ingested food material. Therefore Ashtavidha

Ahara Ayatana, 12 Ahara Vidhi Vidhana should be considered so

that Agni Vaishamya and vitiation of Doshas may not take place.

vii) Ashtavidha Ahara Vidhi Visheshayatana (eight lines for

selection of food)

a. Prakriti (Natural Qualities) – before ingestion of food, the

natural properties of food must be considered so that these may not

hamper Agni and Doshas.

b. Karana (Preparation) – Various cooking procedure may increase

or decrease the properties of food stuffs. This may be due to

admixture of water, heating and predominance of time and season.

Also other factors i.e. Desha, Kala and Bhajana (utensils) must be

considered.

c. Samyoga (Combination) – Charaka has discussed 18 types of

incompatible diet. He has also enlisted various diseases produced

including Amlapitta and Grahani roga due to ingestion of

incompatible diet.

20  

d. Rasi (Quantum) – It refers to the total quality of food as well

as quality of various constituents of diet. Every body must eat

required quality which may directly interfere gastric juice secretion

and digestion process. Atimatra and Amatra Bhojana may lead to

vitiation of Doshas.

e. Desha (Habitat) – This denotes place relating to growth as well

distribution of substance which also direct affect the Agni in

digestion process.

f. Kala (Time) – Here both Nityaga and Avasthika Kala should be

considered. Seasonal dietetic variation, age wise variation, day and

night variation and disease wise variation can be considered.

g. Upayoga Sanstha (rules of use) – This depends on the

digested food.

h. Upayokta – means who consumes the food. i.e. the user. Diet

may vary person to person according to their body compatibility and

habits on him depends the Oka Satmya.

Aharavidhi vidhana (code of healthy eating) –

Charaka has also prescribed the code of healthy eating after

describing the basis for selection of healthy diet which are 12 in

numbers. They are –

i) Ushnamashniyat – It enhances test, increases Agni, easily

digestible and does Vatanulomana and decrease Kapha.

ii) Snigdhamshniyat - It diminishes the Rukshata of ingested food

and regulates the action of Vayu.

21  

iii) Matravadashniyat – Quantity is related with individual’s

Agnibala. Heena and ati qualities of food create the disturbance in

Agni.

iv) Jirne ashniyat – Ingestion of food before digestion of previous

meal cause vitiation of Agni and all the Dosha. Hence meal should

be taken only after digestion of previous meal.

v) Viryaviruddhamshniyat – Intake of Virya Viruddha Dravyas cause

tridosha prakopa.

vi–xi Ekdesha, Ekasarvopakarana, Natidruta Nativilambita Tanmana

Bhunjita Ajalpannahasanam - All the above factors causes proper

digestion of food by which there is no chance of vitiation of Agni.

xii) Atmanam Abhisamikshabhunjita – Every user must consider his

self well. Hence all the above factors are responsible for proper

secretion of gastric juice and digestion occurs. If any one cause

vitiation of Pachakapitta/ Samanavayu leads to Agni Dushti.

Sushruta has also prescribed the code of behaviour after taking

meal. He has advised walking for at least 100 steps. There after

taking rest for sitting position for a while and there lying supine in

left side position. This gives proper time for digestion34.

According to modern

Digestion means the breaking down of larger food molecules

into smaller molecule. The passage of these smaller molecules into

blood and lymph is termed as absorption. So the organs which

perform both these constitute the digestive system. Digestion

includes 6 basis process i.e. ingestion, secretion, mixing and

propulsion, mechanical and chemical digestion, absorption and

defecation.

22  

1. Ingestion – This process involves taking food and liquid into

mouth.

2. Secretion – Cells within the walls of GI tract and accessory

digestive organs secret seven liter of water, acid, buffers and

enzymes within the tract/day.

3. Mixing and Propulsion – Alternating contraction and relaxation of

smooth muscle in the walls of GI tract mix food properly them

towards anus.

4. Digestion – The process of digestion starts from mouth. Two

types of digestion i.e. mechanical and chemical process break down

ingested food into small molecules.

a. Mechanical digestion – Teeth cut and grind food, then smooth

muscles of stomach and small intestine churne the food. So that

food molecules become dissolved and mixed thoroughly with

digestive enzymes.

b. Chemical digestion – A series of hydrolysis reaction that break

down large carbohydrates, lipids, proteins and nucleic acid with the

help of digestive juice (saliva, gastric juice, pancreatic juice, succus

entericus and bile) into smaller molecules that are usable by body

cells.

c. Mechanical Chemical digestion in mouth Mechanical digestion – It

helps the process of mastication of the food stuff and in preparing it

into a bolus and suitable for deglutition. Here saliva acts as

lubricant. Chemical digestion – two enzymes i.e. salivary amylase

and lingual lipase contribute in it. Salivary amylase initiates the

break down of starch, into monosaccharides for which it can be

23  

easily absorbed into the blood stream. Lingual lipase secreted by

glands in the tongue. It breaks down dietary triglycerides into fatty

acids and diglycerides.

d. Mechanical and chemical digestion in stomach Mechanical

digestion – It consists of mixing waves (peristaltic movements) by

which food mix well with secretion of gastric glands and form a

souping liquid called chyme and also these waves pushes the chyme

into duodenum through pyloric sphincter. Chemical digestion –

Gastric juice secretion from the cells of stomach which takes part in

digestion i.e. Cell Secretion Results

1. Chief cells

a. pepsinogen Inactivateform becomes activate with the help of HCl

and breaks down proteins into smaller peptide fragments.

b. Gastric lipase Splits short chain triglycerides into fattyacids and

mono glycerides.

2. Parietal cells

a. 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 mucus

a. Mucus forms a protective barrier that prevents digestin of

stomach wall.

24  

b. Absorption small quantity of water, ions, some drugs enter the

blood stream.

4. G cells

a. Gastrin stimulates parietal cells to secrete HCl and chief cells to

secret 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 and

contraction of stomach wall. Gastric digestion occurs in three

hases. i.e. -

1. Cephalic phase

2. Gastric phase

3. intestinal phase

Cephalic phase: This phase of gastric secretion occurs even before

food enters the stomach. It results from sight, smell, thought or

taste of food, and greater the appetite, the more intense is the

stimulation. Neurogenic signals causing the cephalic phase of

secretion can originate in the cerebral cortex or in the

hypothalamus. They transmit impulses through vagus nerve to

stomach. This phase of secretion accounts for one tenth to one fifth

of the gastric secretion.

Gastric phase: Once food enters the stomach, it excites the gastrin

mechanism, which in turn causes a low rate of secretion of gastric

juice that continues throughout the several hours that the food

remains in the stomach. In addition, the presence of food in the

stomach also causes- i) local reflexes in the intramural plexus of

25  

stomach and ii) vasovagal reflexes that pass all the way to the

brain stem and back to the stomach. Both these reflexes causes

parasympathetic stimulation of gastric glands and add to the

secretion caused by gastric mechanism. The gastric phase of

secretion accounts for more than two thirds of the total gastric

secretion associated with eating a meal.

Intestinal phase: Even after the food has left the stomach, small

amount of gastric juice. Continue to be secreted for six to eight

hours, i.e. As long as chyme remains into the small intestine.

Further more, this secretion will still occur even when all nerve

connections are cut. Further presence of fatty acids and glucose in

chyme triggers enter endocrine cells in the small intestinal mucosa

to release two hormones that affect the stomach ie. Secretin and

cholecystokinin. Secretin mainly decreases gastric secretion

whereas CCK mainly inhibits stomach emptying. Also both

hormones have other important effect on pancreas, liver and Gall

bladder that contribute to regulation of digestive protcess. Only

about 5% of total gastric secretion occurs during the intestinal

phase.

Pancreatic juice:

The enzymes in pancreatic juice digest all the foods i.e.

i) Pancreatic amylase – hydrolyzes starch, glycogen and other

Carbohydrate 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 acid

digesting enzyme.

iv) Pancreatic lipase – hydrolyzing neutral fat into glycerol and fatty

acids.

26  

The above pancreatic secretion are regulated by nervous and

hormonal mechanism.

a. Nervous mechanism starts 1-2 minutes after taking food.

b. Hormonal mechanism starts when stomach empties into

duodenum. Two hormone i.e. secretin and pancreozymin is

responsible for increased secretion of pancreatic enzymes. Bile –

Bile secretion by liver is continuous. Though it contains no digestive

enzyme, but important for digestion because of the presence of bile

salts,

which help –

1. To emulsify by fat globules so that they can be digested by the

intestinal lipase.

2. Render the end products of fat digestion soluble so that they can

be absorbed through the GI mucosa into the lymphatics. Machanical

and chemical digestion in the small intestine. Chyme entering the

small intestine contains partially digested carbohydrates, proteins

and lipids. The completion of digestion is a collective effort of

pancreatic juice, bile, and intestinal juice. Machanical digestion- It

involves segmentation and migrating motility complexes.

Segmentation mix chyme with the digestive juice and bring the

particles of food into contact with the mucosa for absorption.

Migrating motility complex is the type of peristalsis begins in the

lower portion of stomach and pushes chyme forward along small

intestine. Altogether, chyme remains in small intestine for 3-5

hours.

Chemical digestion – various enzymes secretes from the brush

border of the intestine, which also takes part in digestion. These

are-

27  

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 bond

that attaches the terminal amino acid to the amino end of the

peptide.

ii) Dipeptidase – splits dipeptides into single amino acids.

Fat digesting enzyme –

i) Lipase (intestinal) – splitting neutral fats into glycerol and fatty

acid. Digestion of nucleic acids: The nucleotides result from the

action of pancreatic nucleases are further digested by brush border

enzyme called nucleosidases and phosphatases into pentoses,

phosphates, and nitrogenous bases. Mechanical and chemical

digestion in large intestine-

Mechanical digestion – it involves the movements of large

intestine includes haustral churning, peristalsis and mass peristalsis

by 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 the

aminoacids into simpler substances, ie. Indole, skatole, hydrogen

sulfide, and fatty acids.

- It decomposes bilirubine to simpler pigments, including stercobilin,

28  

which give faeces their brown colour.

- It also produces some vitamins i.e. vit. B and vit. K that are

absorbed in the colon.

5. Absorption – The entrance of ingested and secreted fluids, ions

and the small molecules that are products of digestion into epithelial

cells lining the lumen of the GI tract is called absorption. The

absorbed substances pass into blood or lymph and circulate to cells

throughout the body.

6. Defecation – wastes, indigestible substances, bacteria, cells-

sloughed from the lining of the GI tract and digested materials that

were not absorbed leave the body through the anus in a process

called defecation the eliminated material is termed feces.

29  

DISEASE REVIEW

The word ‘Disease’ literary means the lack of ease. According

to Taber’s encyclopedic medical dictionary, disease means “A

pathological condition of the body that presents a group of

symptoms peculiar to it & that sets the condition apart as an

abnormal entity differencing from other normal or pathological body

states.” Amlapitta is a disease which is commonly found almost all

part of world.

Ayurvedic View:

HISTORICAL REVIEW:

To have a complete knowledge of subject it is necessary to

trace out its historical background for the disease Amlapitta one has

to trace out its original concepts various developments at present

stage & the work done on the subject by various research workers.

A) VAIDIC KALA :

In Vedic literature, showed no suggestive references of

Amlapitta description.

B) SAMHITA KALA :

1. Charaka Samhita :

Acharya charaka has not mentioned Amlapitta as a separate

entity but Charaka Samhita has many scattered references of

Amlapitta 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.

30  

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 Amlapitta

where as ‘Mahatikta ghrita & kansaharitaki are prescribed for its

treatment. Hence it can be concluded that during the period of

charka all aspects of Amlapitta disease were considered.

2. Sushruta Samhita

Acharya Charaka has mentioned the word Amlapitta but it is

not found in sushruta samhita. Sushruta has mentioned symptom.

Known as ‘Amlika’ results from excessive use of Lavan Rasa, is

similar to Amlapitta, ‘Amlika’ word has found in sushruta samhita

su. 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

31  

given aetiopathogenesis, clinical features complications &

treatment & also gives suggestion to change the place of living to

have good peace of mind to cure the disease thus in the Upanishad

kala also it was firmly believed that manasika bhavas are affecting

the disease Amlapitta.

4. Harita Samhita

Harita Samhita in 24th chapter of 3rd sthana has described

Amlapitta as a separate disease & given the treatment. It also

gives. 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 Kala

1. Ashtang Sangrah & Hridaya

Vagbhata I & II were one of the most eminent of ancient

physicians who written the Astanga Samgraha & Astanga Hridyam

respectively.

In both these text Amlapitta word & synonyms of Amlapitta

i.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 of

1. 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’.

32  

2. Madhava Nidana

After Kashypa Samhita, Madhava Nidana is first available text

which gives importance to Amlapitta and describes its

aetiopathogenesis & symptomatology in details along with two

clinical subtypes viz.

1. Urdhvaga Amlapitta

2. Adhoga Amlapitta

Vri. Madhav has described Amlapitta is an independent

disease & also its therapy.

3. Chakradatta

In this classics, vamana, Virechana, Basti etc. treatments are

advised for Amlapitta along with its Chikitsa Sutra the

symptomatology of Amlapitta is given the detailed treatment of

Amlapitta is given by Chakradatta.

4. Sharangadhara Samhita

Sha. Sa. Being a book of pharmacoped has given only

Amlapittahara recipes without describing the aetiopathological

concepts of the disease.

5. Basavarajiyam

This text has included the Amlapitta under 24 Nanatmaja

Vyadhi of pitta.

6. Bhavaprakasha

Two separate chapters on Amlapitta has been devoted in this

text. Upadrava & arista are explained in this text.

33  

7. Yogaratnakara

Regarding Amlapitta, he has followed Madhav Nidana totally &

this text has added four more upadravas to list of upadravas of

Amlapitta.

8. Vangasena Samhita

Acharya Vangsena in Vangsena Samhita described Amlapitta

in 59th chapter as “Amlapitta Rogadhikara”.

9. Siddhanta Nidana

Detailed information about Amlapitta is given according

Modern 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 is

described in detail.

D) Previous Research work

On specially Urdhwaga Amlapitta following research scholars

have 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.

34  

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.

35  

AMLAPITTA – AYURVEDIC REVIEW

To know the Ayurvedic view about Amlapitta one must go

through 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 equated

with the sour taste which causes excessive salivary secretion pitta

is a bodily chemical substance which is mainly responsible for the

maintenance of the process of digestion transformation &

transmutation on combining both these words the term Amlapitta

implies to a disease or condition in which the sourness of pitta get

increased.

Paribhasha/Defination

1. Vachaspatyam

According to vachaspatyam, Amlapitta means pitta leading to

sour taste.

2. Chakrapani

36  

Which means that the quality of pitta i.e. sourness when

increase leads to Amlapitta.

3. Vijayrakshita

Commentator of madhav Nidana defines the words as

Amlapitta which means that the pitta having vidahi quality give vise

to Amla or sour taste.

4. Shri Gananath sen in his book sidhanta Nidana has given

similar defintaion of Amlapitta.

The above classical description of Amlapitta emphasises that

Amlapitta is a patho-physiological condition in which the pitta gets

vitiated in terms of Vridhi (excessiveness) & also the sourness of

pitta is increased.

Paryaya/Synonyms

Pramilaka44 – Vagbhat

Pitta visuchika45 – Vagbht

Pittamlaka – Harita

Amlika – Sushruta

Shukta – Kashyapa

Dhumaka46 – Vagbhat

Vargikarana / Classification

1. Madhavkara classified Amlapitta in two ways as follows :

a) According to pravriti : Urdhwaga

Adhoga

b) According to Dosha : Vataja Amlapitta

Vata kaphaja Amlapitta

Kaphaja Amlapitta

37  

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 Kaphaja

Amlapitta can also be classified according to various factors

as follows –

a) Koshthagata – according to its site

b) Nija Vyadhi – according to its aetiology

c) Amasaya samutpanna vyadhi

d) Abhyantara margajaneet vyadhi

e) Doshabalapravritta vyadhi

Nidana / Aetiology

After a careful screening & analysis of the etiological factors of

Amlapitta, 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 under47

Aharaj Hetu (Dietary factors)

The first & the foremost group of etiological factors of

Amlapitta may be considered as the dietary factors. Under this

group the intake of food against the code of dietetics i.e. Ahara

Vidhi Vidhana & Ahara Vidhi Visheshaayatana is included.

38  

Various type of incompatible substance excess of pitta

aggravating factors like katu Amla, Vidahi etc. & irregular time of

consumption of food are the factors against the dietetic code & they

are directly responsible for the annoyance of pitta.

a) Viharaj Hetu (Habit oriented factors)

To maintain the sound & good health one has to follow the

code of habits. He is required to have regular habits of defecation

eating & 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 of

the body. If this is not followed regularly, the whole functioning of

the body will be disturbed & in long run; they will cause the

disturbances of the equilibrium of pitta & digestion which ultimately

will lead to Amlapitta.

b) Manasika Hetu (Psychological factors)

Psychology also plays a great role in maintaining the health of a

person. 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 & by

that, they are disturbing the homeostasis which interns Amlapitta.

c) Agantuja Hetu (Other related factors)

Now a days Gastrogenic diseases are common. Amlapitta could

be a sequel of faulty drug use. Over the counter intake of non

steroidal anti-inflammatory drugs & antico-agulant cure one disease

but it can produce Amlapitta, Ayurvedic drugs specially unpurified &

faulty Rasa Aushadhi may cause Amlapitta. Even Ushna, Tikshna

drug if used excessively without proper assessment of disease for a

long period may produce Amlapitta similarly panchakarmas with

Heenayoga or mithya yoga or Atiyoga lead towards many diseases

39  

by attacking on Agni hence Amlapitta also can be seen as an

Upadrava of some other diseases like chronic Vibandha, Arsha,

Ajirna, Pandu.

1) Ahara group48

a) 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 pana

c) According to the Samskara of the Ahara

Apakwanna sevana

Bhristadhanya sevana

Isksuvikara sevana

Pistanna sevana

d) According to Dusitanna

Dusta anna sevana

Paryusita anna sevana

e) According to the pitta provocative potency of diet.

Adhyasana Ajirnsana Ati drava

Ati Usna Ati Amla

Ati Tikshna Virruddhasana

f) According to the capacity of weakening the digestive power

Ati snigdha sevana

Ati Ruksha sevana

g) Faulty dietary habits

Akala bhojana Antarodakapana

Kala anasana Visamasana

40  

h) Miscellaneous

Annahina madya Madya sevana

Gorasa sevana

2. Vihara Group49

a) Atisnat

b) Ati avagahanat

c) Bhuktwa bhuktwa diwasvapnat

d) Veganam Dharanam

e) Shaiya prajagaran

3. Manasa Group50

a) Chinta b) Shoka c) Bhaya d) Krodha e) Moha

4. Others –

Other factors are –

Ayurvedic drugs especially unpurified and faulty Rasa Aushadhis.

Ushna and Tikshna drugs if used excessively without proper

assessment 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 smell

of certain food items provoke a strong reflex vomiting in which

stomach is powerfully irritated. Also Desha, Kala, Ritu takes a great

extent in the causation of Amlapitta i.e. –

Deshaprabhava: According to Acharya Kashyap the disease is

more predominant in anupa desha comparing to other desha

because of Kapha provocating nature51. In the line of treatment he

gives its importance to change the place in untreated cases52.

41  

Kalaprabhava: Amlapitta is a chirakalina vyadhi this kala or time

factor is responsible for physiological/ anatomical structure of the

body i.e. Balavastha, Madhya and Vriddha Vastha. The disease is

more prevalent in middle age due to Pittapradhanya. Also paittika

disorders are more prevalent during Pitta provocation time that is

during mid-day and mid-night.

Ritu prabhava: This group includes disease which is caused by the

meteorological changes such as variations in atmospheric

temperature, hot or cold, humidity or dryness, rain and winter,

incidental to changes in the seasons. The rainy season is

responsible for amlavipaka of water (due to weakened digestion

power and vitiation of Vata and other Doshas) and eatables, which

in 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 in

families prove relation of genetic factors. Probably the blood group

modifies the oxyntic cell population.

ii) Dietary factors:

Irritant food materials such as rich and spicy diet, hot tea and

coffee, pickles etc. are responsible for stimulation of gastric

secretion.

iii) Trauma:

Due to passage of any solid matter, pyloric obstruction or stenosis

resulting, from cicatrical changes following the ulcers, Chronic

42  

Functional spasm, carcinomia and congenital defects are always

associated with gastritis.

iv) Drugs:

Coricosteroids, xanthine, aspirine, alkaloids, NSAIDS, reserpine are

reported to be the predisposing factor.

v) Neurogenic and psychosomatic factors:

There is a well recognized association between mental stress and

hyperchlorhydria.

vi) Nicotine and alcohol:

Alcohol directly damages the gastric mucosa and produces ulcer.

Smoking has been reported to produce the amount of prostaglandin

E2 in gastric juice and to inhibit prostaglandin synthesis in gastric

mucosa.

vii) Predisposing factors:

Duodenal ulcer occurs specially in energetic ambitious young men

who have irregular and often hurried meals and tend to over work.

Such as in Bus drivers, business executives, medical practitioners

etc.

viii) Endocrine factors:

Emotional and systemic stress can act on the stomach through

hormonal as well as nervous pathway, namely hypothalamus, ant.

Pituitary, ACTH, adrenals, cortisone and gastric glands. (Since

peptic ulcer is more common in males it has been suggested that

estrogen hormones may protect against the development of ulcers.

Moreover, specific endocrine disease or condition have been proved

to be associated with peptic ulcer i.e., excessive adrenocortecal

43  

activity, hyperparathyroidism. Zollinger Ellison syndrome multiple

adenoma syndromes.

ix) Social factor:

It is reported that a markedly increased incidence of gastritis found

in unhygienic and lower social economical classes.

x) Reflexes:

Reflex stimuli from heart, pleura and other organs in the body

may also set up gastric symptoms. Patients having bronchiectasis or

PTB also shows symptoms of gastritis and gastric ulcers. Stress

ulcer i.e. Curling and Cushing ulcer are included under peptic ulcer.

In Curling ulcer excessive burn of skin cause more secretion of

adrenaline and noradrenaline which mixed with circulation and

stimulate HCl Producing gastroduodenal ulcer. Whereas in Cushing

ulcer raised intracranial pressure due to head injury causes

stimulation of parasympathetic responsible for increased secretion

of HCl lead to peptic ulcer.

Infection: Helicobactor pylori plays a significant role in developing

gastritis also a number of viral, fungal and other bacterial infection

were accompany by gastritis.

Samprapti:

According to Ayurvedic concept, for the proper manifestation of a

Disease the vitiated Doshas and dushyas unite in several stages.

These stages are known are Kriyakalas, which mean, it guides the

proper time for treatment at a particular stage of Doshika imbalance

in a given disease. Various stages is very necessary for early

diagnosis as well as for prompt treatment and for adopting

prophylactic measures at the onset. Therefore, in explaining the

44  

samprapti, it is very appropriate and logical to take the Sushruta’s

concept 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 a

particular and a special pattern which is called the melaka vishesha

or end product of Dosha dushya samurchhana. Similarly in the

manifestation of all diseases, Dosha, dushya and malas are the

common factors also some other factors are responsible i.e.

Rogamarga, Adhisthana, Sanchara, Udbhava, Agnimandya, Ama

and Strotas. Samprapti ghataka is necessary before starting to

discuss 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

45  

Vyadhi – Amashayotha

Rogamarga – Abhayantara rogamarga

Paradhanta – Pitta dosha pradhanya

Prabhava – Daruna

Dosha- In pathophysiology the involved sites of lesion and

disturbance are Pachaka Pitta, Samana Vayu and Kledaka Kapha.

Samana vayu – It controls all the secreting and motility functions

of the two Ashayas and helps in the action of digestive enzymes,

assimilation of end products of food and their separation into

various tissue elements and when vitiated, it causes indigestion,

diarrhoea and defective assimilation.

Pachaka Pitta- The Amlaguna and Dravaguna of Pachakapitta get

vitiated. Kledaka Kapha situated in amashaya is to counteract the

destructive action of Pachaka Pitta. Due to imbalance of Pitta the

Pachana Kriya is also disturbed. This leads to the formation of

Vidagdhajeerna then to Suktapaka and later to Ama.

a. The term ‘Ama’ means Apakva Annarasa. If Anna is not properly

digested then the out come of such an Apakva Rasa is Ama.

b. Due to impairment of Kayagni. The Annarasa is not properly form

and in this state, it is known as Ama.

c. The undigested Annarasa possessing foul odour and excessive

stickness deprive the body of its nutrition causes sadana. This sticky

substance is known as Ama.

46  

e. Due to poor strength of jatharAgni residue of ahara rasa is still

left behind undigested towards the end of digestion. It is ama which

is 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 or

saptadhatus or with malas. Then they are called Sama. The disease

produced is also called as Sama rogas.

Symptoms of Sama Doshas –

Samavata Samapitta SamaKapha

Vibandha

Stambha

Antrakunjaam

Vedana

Shopha

Nistoda

Adhmanam

Asanchara

Durgandhi

Haritam Shyavam

Amlam

Ghanam

Guru

Amlikarkaram

Kantha-Hrid

Dahakaram

Avila

Tantula

Styana

Pralepi

Pichhila

Kandhdeshe

Avatishthate

Kshudrudgaravigh

atakara

Agni – Sushruta explains that the prana, samana and apana while

remaining at their original sites maintain Agni54. The vitiation of any

one of these may lead to Agni dushti and sometimes vitiation of

Agni may lead to disturbance in function of these three or any one

of 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 Agni

may start the pathogenesis i.e. Vishamagni, ii) Tikshnagni and iii)

Mandagni, which are said to be the work of tridosha. As the disease

47  

of GIT are caused due to Agni Dushti, hence, all the three doshas

may affect the Agni but the manifestation may be according to the

dominance of three Doshas. Kashyap Samhita is the first which

explains the symptoms of Amlapitta according to involvement of

predominat Doshas.

Srotas – The disease involve Amashaya, Grahani and Pakvashaya.

Hence Anna and Purishavaha Srotas seems to be mainly concerned

but the Rasavaha Srota which receives the first Ama Visha produced

due to Agni Dushti may get involved. Regarding the types of

Srotodushti the three types of disturbance of Annavaha and

Purishavaha can be observed i) Sanga, ii) Atipravritti and iii)

Vimarga Gamana.

Dushya – While reviewing the symptomatology of Amlapitta and

Grahani, it seems that the main Dushya may be Rasa. This is the

first dhatu to receive the Ama Anna Rasa. The aetiological factors

and symptomatology is also suggestive of Rakta Dushti.

Mala – “Na Vegan Dharyet”

Ayurved gives one of the most important cause of diseases

according to Ayurvedic conceptualization is Vegavarodha i.e.

suppression of natural urges.

eg. Micturation, defaecation, hunger and sleep, etc. This supression

of natural urges affects the sphincteric competence adversely.

Natural contractility and motility of smooth muscles of various

viscera, the GI tract and the macro and micro channels of the body

are also affected adversely. Once the sphincter of various srotas or

channels get affected, it leads to abnormality in them leading to

accumulation and later vitiation of Doshas.

48  

Samprapti of Amlapitta

In vrihatrayee, the disease has not been mentioned in detail but in

Charaka samhita the Amlapitta terminology is used at various

places. Though Charaka has not mentioned it as a separate disease

entity, but in the context of grahani chikitsa he has explained the

etiopathogenesis of disease. The etiological factors like Abhojana,

Atibhojana, Veganigraha, Panchakarma Vyapat and seasonal

variation etc. cause vitiation of Doshas and Agni which ultimately

results Mandagni which is treated as mother of all the diseases. This

Mandagni leads to Avipaka and due to Avipaka even light and small

meals are not digested. This undigested and ill digested food gets

shuktatva which leads to the formation of Annavisha. This

Annavisha 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 properly

digested it gets formented and forms Annavisha. This Ama when

mixed with Pitta then it develops the disease Amlapitta. Usually

Dravaguna and Amlaguna of Pitta vitiates causing Vidagdhajirna at

the initial stage. If neglected as suggested in Siddhanta Nidana57.

This will progress causing inflammation and erosion of

sleshmadhara kala of amashaya leading to manifestation of Grahani

Roga.

49  

Kriyakala –

Sanchaya – Stage of Agni dushti may be described as the stage of

sanchaya i.e. Due to Sanchaya of Pachaka Pitta, Samana Vayu and

Kledaka 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. The

symptom 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 doshas

with Visharupa Annapana. Also it is noted Manovaha srotas gets

vitiated due to excessive manifestation of various mental factors

causing symptoms of Ajirna and Amlapitta.

Sthana sanshraya – This is the further stage and from here the

specific pathogenesis of each disease starts according to the

specificity of Nidanas, quality of Doshas by which they are vitiated

and the place of khavaigunya. So, the three Doshas Samanavayu,

Pachaka Pitta and Kledaka Kapha may get Sthana Sanshrita in

Amashaya (including Grahani) where simultaneously khavaigunya

might have been produced by the same nidanas or by any other

nidana. The symptoms produced in this stage may be same as

symptomatology of the Amlapitta and having less severity. If

tratement is not done in this stage the pathogenesis may proceed

further and may produce the disease like Parinama Shula. This is

the stage from where the Vidagdhajirna can be separated from

Amlapitta. Vidagdhajirna is an acute stage occurring due to nidanas

directly. And is Nidana Sapeksha, which means after the

Mithyaahara Vihara of Pittaprakopa diet articles will lead to

vidagdhajirna, but here the Doshas have not established their

affinity with any organ on tissue and only langhana or time will cure

50  

the condition, but symptoms may be produced again and again

whenever the Mithyaahara and vihara will be done. But due to again

and again provocation, the Doshas will establish their affinity in

Amashaya and Grahani (sthanasamshraya). After this stage even

the laghu and Alpa Bhojana will cause shuktatva and Vidagdhata to

Annapana leading to the production of Amlapitta Roga.

Vyakti – At this stage the symptoms of disease Amlapitta may get

well established and further differentiation in Doshik varieties

according to predominance may be established. The three Doshik

predominant subtypes of Amlapitta have been advocated by

Acharyas i.e. Vatika, Kaphaja and Vatakaphaja. Madhavakara has

also given a separate classification according to the expulsion root

of Doshas i.e. Urdhvaga and Adhoga types.

Samprapti of Amlapitta (interms of Charaka)

1. Sankhya samprapti

a. Two types according to Gati.

i. Urdhvaga

ii. Adhoga

b. Three types according to Kashyap

i. Vatolvana

ii. Pittolvana

iii. Kapholvana

c. Three types according to Madhavakara

i. Vatika

ii. Vata kapha

iii. Kapha

iv. Also counted fourth types as shleshma Pitta

51  

2. Vidhi Samprapti –

a. i. Nija ii. Agantuka

b. i. Svatantra ii. Paratantra

c. According to curability –

i. Naveena - curable by tactful persuation

ii. Chirothita - krichhra sadhya

iii. Chirothita – yapya

3. Vikalpa samprapti –

i. Vata - Chala, Ruksha, Karmatah

ii. Pitta - Dravyatah, Ushma, Tikshna, Sara, Amla, Katu, Drava

iii. Kapha - Dravyatah, Karmatah, Guru, Mridu.

4. Pradhanya samprapti –

i. Pitta - Vriddhatama

ii. Kapha - Vriddhatara

iii. Vata – Vriddha

5. Bala – kala vishesha

a. Seasonal aggravation i. Sharada ii. Greeshma

b. Day/ night i. Noon ii. Mid-night

c. Dietetic time i. Bhojanottara

Bheda – When the disease progresses further it reaches to sixth

stage. Due to the manifestation of various symptoms, the disease

can be categorised as Vatika, Vata Shleshmika or Shleshmapitta as

described by Madhavakara. Due to further involvement of Vata and

Rakta, the disease can produce Parinama Shula, as a Upadravas or

as Nidanarthakaratva.

52  

SHADAVIDHA KRIYAKALA OF AMLAPITTA

Kriyakala Name Treatment

Use of Ahara without following the Ashtavidha Ahara Ayatana and Asana Pravichara Agnidushti I Sanchaya NidanaParivarjana

Ajirjna II Prakopa Langhana

Further 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 disability

Doshik type of manifestation Upadravagamana Amashayagata Rakta VI Bheda Rehabilitation Pakvashayagata Rakta Bhinna Koshta

Further manifestation of symptoms of Amlapitta

Doshik variance Upadrava Rupata

53  

Swatantra and paratantra status of Amlapitta –

The above pathogenesis described for production of Amlapitta

shows that this is a Paratantra Vyadhi produced by one another.

But Swatantra type occurs, due to the potency and

multiplicity of Nidanas, diminution of Vyadhi, of

Utpadapratibandhaka Shakti and due to such other reasons,

Amlapitta may be caused directly. Hence if the nidanas are so

strong it causes vitiation of Doshas and Dushya, producing Shotha

in Pitta Dhara Kala of amashaya and grahani lead to occurance of

Amlapitta roga.

Different opinions regarding samprapti of Amlapitta-

Acharya Kashyap was the first to analyze the disease on

Doshik basis, he described the samprapti in detailed. He believed

that (the disease caused by vitiation of three Doshas (Vatadayah)

causing Mandagni leads to Vidagdhajirna manifesting as Amlapitta.

Whereas Madhavakara describes the development of Amlapitta due

to vitiation of pitta which is already increased due to its own cause.

Also Kashyap considered Apakva Madya and Dugdha as causative

factor, whereas Charaka lists Dugdha as one of the pathya for

Amlapitta. Harita counts Guda as the causative factor for Amlapitta.

In the management, single drugs like Haritaki, Pippali and Rasona

were advised by Kashyap whereas Kapittha, dadima and dhatri

advised by other of Yogaratnakara among the comound drugs

‘Narikela Lavana” suggested by author of Rasatarangini, Narikela

Khanda, soubhagyasunthi, Shunthi Khand suggested by Bhaisajya

Ratnavali etc.are the good remedies for Amlapitta. On analyzing,

the pharmacodynamics of these above drugs proved effective in the

management are contraindicated in increased Pitta condition.

54  

Where as the drug of choice should be tikta and madhura rasa

pradhana. Even present day scholars have ventured on research on

effect of drug like Amalai, Shatavari, Madhuyukta, Guduchi,

Bhringaraj, Patol, Pippali, Puga, Udumber etc. in the management

of Amlapitta. That’s why Doshik predominance has been considered

and stressed on the classification according to Kashyap and even by

Madhavakara.

Why pitta kapha classification considered not Vata?

a. Acharyas decribed that diseases are not produced due to any

single Dosha but by all the three Doshas58. Also they explained that

non-compliance of healthy eating causes the vitiation of three

Doshas simultaneously. So, whenever Annavisha mixed with

Samsrijyamana Pitta (Pitta predominant Tridosha). It will causes

Paitika disorders. In the same way whenever Annavisha mixed with

Vatasamshrista and kapha Samshrista (Vata predominant and

kapha predominant tridosha).

It leads to Vataja and Kaphaja disorders respectively. So, all the

disease produced are Tridoshajanya.

b. Madhavakara explained that Pitta is responsible for the

pathogenesis of Amlapitta, but the Nidana like Viruddha Ahara has

been enlisted which is said to be the causative factor of three

Doshas.

c. Samanavayu, Pachaka Pitta and Kledaka Kapha may get Sthana

Sanshrita in Amashaya. And these have various relation ship. When

vitiation of any one, may disturb the others. Kledaka Kapha protects

the amashaya by counteract the secretion of Pachakapitta. Also

Samana Vayu maintains / balances the Agni and proper digestion.

So when Vata gets vitiated, it seems the possibilities due to

55  

margaavarana from Pitta and Kapha. Hence Amlapitta is a disease

condition produced due to Pitta Kphavrita Vata.

d. Kanthadutta has classified that like Kotha, the causative factors

of Amlapitta are kapha and pitta. He has further clarified that

though the pitta is chief Dosha in Amlapitta, Gaurava, Udgara and

Kampa symptoms are due to Kapha and Vata respectively. Hence it

is 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 Kapha

and adho Amashaya is the seat for Pitta. Hence Kapha and piita

predominace should be considered due to the predominace. There is

more chances of involvement of local factors in pathogenesis

process.

f. Acharya Kashyap quoted the Doshas as ‘Vatadayah’ but later he

has stressed that the dominant Doshas are Pitta and Kapha59.

SAMPRAPTI

The word samprapti is the process of disease formation

beginning right from the contact of the causative factor with the

body to complete manifestation of the symptoms. It is a course

followed by a disease in which a Dosha get vitiated & the path it

follows for the manifestation of disease. The same idea is reflected

by the word pathogenesis used in the modern medicinal sciences.

Kashyap, Madhava & Gananatha sen have mentioned specific

Samprapti of Amlapitta as follows.

Over indulgence in above mentioned factors cause vitiation of

vata & pitta doshas Anyone of the involved doshas slackens

56  

jatharagni (to below normal level) i.e. jatharagnimandhaya. During

the 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 Vidhagadhajirna

manifests which is the purvarupa of the disease Amlapitta.

Further vitiated pitta get mixed with shukta & causes pitta

Ama Visha samurchhana. The disease Amlapitta with its cardinal

symptoms is then takes place.

If not treated properly in this stage the disease leads to

Bheda avastha where the typical Characteristics & types like

Urdhavagata & adhogata are differentiated.

Further, complication like shita pitta, Udarda, Kotha, etc. are

differentiated.

57  

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 prakopa

Vidagdhavastha 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

58  

Purvarupa

In Ayurvedic classics, no specific purvarupas of Amlapitta are

mentioned but by applying tarka & pratical knowledge some

important inferences can be drown.

As already explained in the sampropti Agnimandya & Ajirna

are the successive stages towards the manifestation of Amlapitta.

Also they are practically observed in the patients. Annavaha &

purishavahasrotodusti symptoms can also be considered as

purvarupa of Amlapitta.

Rupa

Rupas or Lakshanas are useful for the clinical knowledge of a

disease symptomatology of Amlapitta has been described by

Kashyap, Madhavakara and Harita. Later workers of Sangraha kala

viz, Bhavamishra, Vangasena, and Yogaratnakar have blindly

followed Madhavakara in this regard Basavarajiyam has included

Amlapitta in the Nanatmaja diseases of Pitta and given three new

symptoms i.e. Swarahinata, Vak-jihva Paridosha. The general

symptoms of

Amlapitta described by madhavakara as follows53.

- Avipaka - Tikta-Amla Udgara

- Gaurava - Klama

- Utklesha - Hritdaha

- Aruchi - Kanthadaha

Kashyap added extra symptoms like –

Antrakujana

Udaraadhmana

Vidbheda

Hritshula etc.

59  

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 being

presented 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 + - - - - -

60  

Symptoms of Ekadoshaja Amlapitta

Symptoms K.S. H.S. M.N. B.P. Y.R. S.N.

Vatika

Angasada + - - - - -

Jrimbha + - - - - -

Shula + - - - - -

Snigdha Upasaya + - - - - -

Paittika

Bhrama + - - - - -

Sitaupasaya + - - - - -

Svadupasaya + - - - - -

Vidaha + - - - - -

Sleshmika

Chhardi + - - - - -

Guruta + - - - - -

Ruksha Upasaya + - - - - -

Usma Upasaya + - - - - -

Vatadhikya Amlapitta

Bhrama - - + + + +

Cimcimatva - - + + + +

Gatra Sada - - + + + +

Harsha - - + + + +

Kampa - - + + + +

Murccha - - + + + +

Moha - - + + + +

Pralapa - - + + + +

Shula - - + + + +

Tamodarshana - - + + + +

Kphadhikya Amlapitta

Aruchi - - + + + +

Agnimandya - - - - - +

61  

Gaurava - - + + + +

Jadyata - - + + + +

Kandu - - - - - +

Kaphanisthivana - - + + + +

Lepa - - + + + +

Nidra - - - - - -

Sada - - + + + +

Sheeta - - + + + +

Vami - - + + + +

Pitta – Sleshma Amlapitta

Amlodgara - - + + + -

Aruchi - - + + + -

Alasya - - + + + -

Bhrama - - + + + -

Chhardi - - + + + -

Hritdaha - - + + + -

Kanthadaha - - + + + -

Kukshidaha - - + + + -

Murchha - - + + + -

Mukha Madhurya - - + + + -

Praseka - - + + + -

Shiroroga - - + + + -

Tikta-udgara - - + + + -

Vishishta Lakshana of Urdhvag Amlapitta

Symptoms K.S. H.S. M.N. B.P. Y.R.

Abhuktevami - - + + +

Abhukte va tiktavami - - + + +

Abhuktetiktaudgara - - + + +

Abhukteamlavami - - + + +

62  

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 - - + + +

63  

Adhoga Amlapitta

Symptoms K.S. H.S. M.N. B.P. Y.R.

Analasada - + + + -

Anga pitata - + + + -

Bhrama - + + + -

Daha - + + + -

Harsha - + + + -

Hrillasa - + + + -

Murchha - + + + -

Moha - + + + -

Vividhapradosa - + + + -

Adhoyan - + + + -

Trita - + + + -

Sweda - + + + -

Kotha - + + + -

64  

SAPKESHA NIDANA

LANDSCAPE PAGE TABLE

65  

Upashaya – Anupashaya:

These factors provide a diagnostic aid for the disease which are

otherwise difficult to diagnose. Specific description about upashaya

and anupashaya is given only by Kashyap while describing Doshaja

types of Amlapitta.

Vataja Aamlapita – Snigdha Upashaya

Pittaja Amlapitta - Swadu and Shita Upashaya

Kaphaja Amlapitta - Ruksha and Ushna Upashaya

Upadrava –

Complications of Amlapitta have not been described by

ancient Acharyas except Kashyap. He has mentioned Upadravas and

stated that the disease is incurable in their presence. Also Acharya

Gananath 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 of

Amlapitta, but included shoola in its vatika predominant variety.

Hence, Parinama and Annadrava Shula can be taken as

complication of Amlapitta.

66  

Shadhya asadhyata –

Madhavakara has pointed out that, if the disease is of recent

origin. It can be cured with proper efforts. In chronic condition

recurrence occurs where treatment is stopped. In some patients it

becomes more difficult to cure even with proper treatment, so the

disease becomes sukhasadhya when it is of short duration, Yapya

when it is chronic and kruchhrasadhya when the duration of disease

is long and cured with great difficulty60. Kashyap has indicated that

if it is accompanied with other Upadravas and Dhatu Kshinata then

it becomes Asadhya61.

Chikitsa

Ayurveda has emphasised 3 basics of chikitsa regarding all

types of diseases.

i. Nidana Parivarjana - It is to be advised the patient to avoid

such aggravating factors of ahara and vihara which are responsible

for causation of the disease. So only wholesome and beneficial

dietetic articles are to be provided along with compliance Aharavidhi

Visesayatana..

ii. Apakarshana – Apakarshana mean pacification of Doshas either

by Shodhana or Shamana or by both. So far Amlapitta is concerned,

it is originated in Amashaya and mostly the Doshas are localized

there. For this condition Vamana is the best treatment. If Doshas

are localized in Pachyamanashaya, then Virechana is the ideal

therapy. In Shodhana therapy Vamana is advocated in Urdhaga

Amlapitta and Virechana in case of Adhoga Amlapitta use of

Niruhabasti is stated by Chakrapani, Vrinda Madhava and Govind

Das. Whereas Vangasen and Yogaratnakar has mentioned the use

of Raktamokshana.

67  

iii. Prakritivighata – It means use of drugs resuscitation of

Dhatus. Such treatment is termed as shamana therapy. Hence

drugs having Pitta/ Kapha shamaka property according to

predominant Doshas have been prescribed but these drugs should

be good for Rasa, Rakta and Annavaha Srotas.

Prakruti vighata means the sanshaman chikitsa the root of the

disease must be ruled out for curation and it can be possible with

the help of prakrutivighta. Without sanshodhan karma, only

sanshaman may help for removing the vitiated Doshas. The drug

that removes the vititation of theDoshas and not expulses it from

the body is called as sanshman karma62 shansaman chikitsa brings

the imbalance Doshas in to its normal position.

- Kashaypa has mentioned following sanshaman chikitsa in

Amlapitta.

(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 responsible

for Amlapitta Langhana is best receipie for removing the Ama Dosha

and Ajirna, Langhana in crease the Agni and so, the root cause of

Amlapitta will be ruled out.

* Laghu Bhojana :-

If the Ahara that taken by the pition digest easily it is called as

laghu bhojana. Laghu Bhojana are not creat Mandagi and Ajirna.

68  

* Satmaya kala & Desha sevana :-

For the pt. of Amlapitta, sharad Ritu, varsha ritu and Anupa Desha

are Astmya these seasions and Desha are responsible for

aggravation if the dis. process. So, releving of these factors must be

necessary. They lead to exaggarate the pitta Dosha63.

* Pachana Karma with shamana Yoga :-

Ama pachana is necessary in Amlapitta. Pachana karma has also a

role 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 the

dominating Dosha, Vamana should be first administered.

b. After Vamana, Shamana drugs should be used. At the same time

Pachana drugs should be given.

c. When the Samsarga Doshas are elevated and stomach becomes

clear, deepana drugs should be administered.

d. If Doshas have shifted into pakwashaya, virechana and

shamasana drugs should be used to eliminate the dhoshas.

Drugs used in Amlapitta

a. Common drugs (herbal)

Ativivisha Shatavari Parpataka

Musta Amalaki Dhanyaka

Trayamana Yastimadhu Hingu

Patola Bhringaraja Narikela

Guduchi Vasa Kusmanda

Kiratatikta Nimba Yavasa

Trivrita Pippali Arka

Triphala (Haritaki) Rasana Vidanga

Danti Udumbara Draksha

69  

b. Rasa Dravyas

Shankha Shilajita Shukti

Abhraka Mandoora Swarna

Lauha Raupya Gandhaka

Swarnamakshika Parada Varatika

Kaparda Manahshila

c. 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 Amlapitta

is suggested by various ayurvedic scholars.

Ahara –

i. Annavarga – Yava, Godhuma, Purna Sali, Mudga Yusha, Lajja

Saktu.

ii. Saka varga – Karavellaka, Patola, Kushmanda etc.

iii. Phala Varga – Dadima, Amalaki, Kapittha, Mrudivika, etc.

iv. Dugdha varga – Godugdha

v. Mamsavarga – Jangala, Mamsarasa

Vi. Haritvarga – Palandu, Pipali, Haritaki

vii. Miscellaneous – Sarkara, Madhu, Marikela Udaka

Vihara –

Shitopachara, Vishrama etc.

Apathya –

i) Ahara – Guru, Vidahi, Viruddha, Kulatha, Udada, Navanna, Tila,

Fermented Foods Like Bread.

ii) Vihara – Vegavidharana, Atapasevena, Chinta, Krodha, Shoka

70  

MODERN REVIEW

Anatomy of stomach

Stomach is the most dilated part of the digestive tube. It lies

in the epigastric, deft hypochondrium & Umbilical regions, the basic

Anatomical subdivisions of the stomach correlated with histological

appearance of Gastric mucosa in different regions. (D1, D2, D3, D4

are 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 unstriped

muscle 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.

71  

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 into

the portal vein.

Nerve supply66:- i) Sympathatic

ii) Para Sympathetic supply is via Vagus.

Sympathetic stimulation causes i) Vasoconstriction of gastric blood

vessels.

ii) Relaxation of gastric muscles.

The position of Prasympathetic stimulation.

72  

G cell- gastrin- parietal cell- HCI

Direct stimulation- parietal cell- HCI

ECl – Histamine- parietal cell – HCI

Mucius cell- mucus

Stimualtion vagal fibers

Leads to stimulation

Chief cell- pepsin.

Vagal parasympathetic stimulation cause rise of HCI

secretation by- a) direct stimulation of parietal cell. b) Inhibition of

somatostain secretion. c) via Gastrin release peptide stimulation of

Gastric 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 in

healthy 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 is

strongly acidic with PH – 0.9 to 1.5.

73  

Functions of the individual compounds of the gastric

secretions.

Secretions Function

1) 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 secretions68

Stimulation Action

Histamine (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

(ACH)

It combine with ACH receptor of the parietal cell

leading to parietal cell stimulation to secrete

HCI.

74  

Inhibition of HCL Secretions69.

Inhibation Action

Prostaglandions It act through inhibilary G proteins that decrease

the generation of cyclinic adenosine

monophosphate

Somatostain 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

75  

Effect of Drug on Gastric acid secretion71

Reduction Neutralization

1) H2 antihistamines :

i) Climetidine, ii) Famotidine etc.

2) Proton Pump inhibitor-

1) Omeprazole, Lansoprazole

3) Anticholinergics-

i) Pirenzepine ii) Propantheline

4) Prostaglardi analogues:-

Misoprostol, Enprostil.

Antacid-

a) Systemic: I) Sodium bicarbonate

b) Non Systemic – Mag. Hydroxide,

Mag.trisilicate

Measures to control Gastric acidity.

No Mesurers

a) Neutralizing Gastric acid using Anatacids.

b) Inhibiting Gastric acid secretion with drugs.

c) Cessation of smoking

d) Withdrawl of Gastric acid secretion stimulants such as alcohol, caffeine &

soft cold drinks.

e) Surgical treatment such as partial Gastroctomy or Vagotomy

76  

MODERN VIEW

It is very much essential to co-relate the disease which are

mentioned in the classics with the recent disease of modern

medicine for a better comprehension of the pathogenesis. In

modern medical literature, some technical terms have been used to

indicate an abnormal condition resembling to Amlapitta. These

terms either explain the pathological condition of the disease or

explain 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 RELATED

1962 Tripathi Gastritis syndrome

1968 4th national seminar on

Ayurveda

i. Sri Purushottam Vaidya Acute Gastritis (Pitta vitiation)

ii. Vd. Vishwanath Dwivedi Chronic gastritis

1982 Tripathi S N Non – ulcer dyspepsia

1986 Harinath Jha Hyperacidity

Also a conference of Vaidyas held at Hrishikesh, has decided

the condition like hyperacidity, hypoacidity, gastritis, gastric

atrophy, gastric and peptic ulcer, gastric carcinoma etc., can be

included in Amlapitta.

Hyperacidity – This word is composed of two components i.e.

hyper and acidus. Hyper means over or excess and acidus means

sour. So a straight meaning may be derived as excess of acid i.e.

77  

any acid not particularly the HCl in stomach and a disease which

contains this abnormal pathology is defined as hyperacidity.

Hyperchlorhydira – This indicates the condition in which there is

an excessive production of HCl in the stomach. It is a characteristic

observation in certain forms of dyspepsia particularly associated

with duodenal ulcer. It causes heartburn and water brash.

Dyspepsia – Indigestion is a collective term for non specific

symptoms though to have originated from the upper GI tract.

Symptoms –

i) Upper abdominal pain or lower chest pain with or without

relation to food.

ii) Regurgitation

iii) Heart burn

iv) Water brash

v) Anorexia

vi) Nausea

vii) Vomiting

viii) Bloating, belching, flatulence

ix) 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 a

new concept that patients have been both hyper and

hypochlorhydria shows the same sign and symptom of Amlapitta.

And they have concluded that Amlapitta is nothing but gastritis

syndrome.

Gastritis syndrome –Gastritis means inflammation of gastric

mucosa where as syndrome means a condition which is associated

with different types of symptoms. The term refers to the nature of

78  

the disease as an assemble of symptoms resulting out of

pathophysiological condition of the stomach.

Gastritis – Gastritis refer to inflammation of the gastric mucosa

which is not a single disease but rather a group of disorder that all

induce inflammatory changes, differ in their clinical features,

histological characteristics and causative mechanism. Several

classifications are as below –

Classification of Gastritis72

A) ACUTE GASTRITIS

1) Acute H. Pylory gastritis

2) Other acute infective gastritis (bacteria, viruses, fungi, Parasites)

3) Actue non- infective gastritis

A) 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 gastritis

Acute Gastritis73 :- It consists of a sudden derangement of

digestion due to inflammation of the mucosa of the stomach.

Aetiopathogenesis74 1) Diet & personal habits : a) Highly

spiced 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. Viral

hepatitis.

3) Drugs:- Intake of drug like Aspirin, Cortisone, Phenylbutazone,

Indomethacin, prepartions of iron, chemotherapeutic agents.

79  

4) Chemical & physical agents :- a) Intake of corrosive chemical

& Physical agents such as Caustic soda, Phenol, Lysol. b) Gastric

irradiation 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 actue

infections, 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 called

as atonic or nervous dyspepsia.

80  

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 appetite

is usually diminished, it may be good but ceases quickly after

beginning the meal. 3) Bad taste in the mouth, the tongue is

flabby, dry & indented by the teeth. 4) There is tendency to

eructation & heart burn, nausea, even vomitting may occur but not

frequently. 5) There are languor, headache, depression, disturbed

sleep, fatigue, discomfort & drowsiness after meals. There may be

palpitation dyspnoea & other cardiac symptoms sometimes acne

rosacea & urticaria.

Description & types of chronic Gastritis:-

A) Types A Gastritis (Autoimmune Gastritis)79 :- It involves

mainly the body fundic mucosa. It is also called autoimmune

Gastritis due to the presence of circulationg antibodies and is

sometimes associated with other autoimmune diseases like

Hashimoto’s thyroids & Addisons diseases. As a result of antibodies

against parietal cell & intrinsic factor there is depletion of parietal

cell & impaired secretion of intrinsic factor due to which there may

be Gastric atrophy or pernicious anaemia.

A) Type B Gastritis (H. pylori related)80 :- This is more common

and mainly involves the region of antral mucosa. It is also called as

Hyperscretary Gastritis due to excessive secretion of acid,

commonly due to infection with H. pylori.

81  

B) Type AB Gastritis81:- This Gastritis affects the mucosal region

of A as well as B type & is most common type of Gastrits in all age

group.

This is also called as environmental Gastritis because a

number of as yet unidentified environmental factors have been

implicated in its aetopathogenesis and chronic Atopic Gastritis

because in advanced stage, there is progression from chronic

superficial Gastritis to chronic Atrophic Gastritis.

C) Alcoholi Gastritis82 :- It is produced by persistent dietetic

errors, especially alcoholic excesses and is aggravated by the

change in the esophagus and venous congest on arising from

cirrhosis of the liver.

E) Erosive Gastritis83 :- This is caused by agents which disturbs

the gastric mucosal barrier. NSAID’s & alcohol are common causes.

F) Acid Gastritis84 :- It is also called as Acid dyspepsia or

Hypochlorhydria.

Causes:- It is due to causes which bring about directly or reflex

excessive 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 the

discomfort does not come on soon after a meal, is followed by

82  

vomiting of acid fluid & is relived by food & by alkalies. The

discomfort consists of sinking feeling in the epigastrium or hunger

pains. 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 life

wretched 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.

83  

Consequences of long term H. Pylori Gastritis88

Description of diagnostic Test:-

Gastric Analysis Test

Gastric analysis denotes an examination of the gastric

contents at various phases of digestion.

Rehfuss in 1914 introduced a method for Gastric analysis or

Fractional test meal which once upon a time was very popular and

routinely done in cases of Peptic ulcer to see whether there was

Hyperacidity or Hypoacidity or Achlorhydria and so on89.

This is rather old and not used these days. Gastric analysis

involves the collection of stomach contents by Ryles tube in fasting.

This is followed by a gastric stimulation, giving a test meal (wheat

bread, rice gruel etc.). The stomach contents are aspirated by Ryles

tube 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 following

conditions.

1) For the diagnosis of disease of the stomach and Duodenum..

2) In clinically suspected cases of Zollinger Ellison syndrome,

Gastric atrophy, Menetriers disease.

84  

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 secretion

2) Motor function:- Resting juice volume, presence of food

particles emptying time of the test meal.

B) Information about intragastric disease:-

a) Presence of blood (Macroscopic, Macroscopic occult) b) Gastric

mucus (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:-

85  

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 obtained

by aspiration through a nasogastric tube. The best recover gastric

secretation is obtained with the patient, in sitting, position patient’s

nostril and throat are sprayed with a solution of 3% Lignocaine in

isotonic solution. A nasogastric tube which was ryles tube previously

and now it is plastic radio opaque 125cm. long tube with holes close

to the tip is first well lubricated with liquied paraffin & is passed

through the nose. The pt. is asked to swallow repeatedly while the

tube is being pushed steadily and rapidly down through the pharynx

and esophagus into the stomach. When a total of about 56cm. of

tube has been pushed the tip is in the stomach, it is confirmed by

aspiration of gastric juice.

C) Aspiration of fasting sample: - 20 ml syringe attached to the

tube & gastric contents should completely emptied by aspiration.

The sample is labelled as ‘fasting’ Washing the stomach with about

20 ml. of distilled water, ensures complete emptying, this washing

sample 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

86  

diagnostic examination of stomach by roentgenoscopy or by

chemical analysis later of gastric contents.

In this clinical study we adopted ewald test meal in which

plain wheat bread 35gr. And water 300 to 400 ml is given through

the mouth95.

An hours later the stomach contents were removed

completely, gastric content is gently aspirated after 15 min., about

10 ml is collected in a clean dry test tube. The procedure is

repeated every 15 min. & 10 samples are collected.96

Examination of gastric contents97 :- Routinely the samples are

examine 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.

87  

Chemical Examiantion:- HCI of the Gastric juice is the component

of chief diagnostic intrest. The juice in addition to other constituents

contains free HCI. It makes the reaction of the gastric juice

markedly acidic. Chemical examination of gastric contents both the

fasting, interdigestive as well as after test meals are of paramount

importance. These examination includes test for free acid total

acid98.

A protion of the acid combines with proteins or protein like

substances. The protein salts of HCI so formed are known as

combined acid. The HCI which remains in excess is known as free

acid of free HCI.

Total acid:- It is defined as the amount of standard alkali required

to titrate 100ml. of gastric juice to PH 8.5 The peak total acidity

may be as high as 70-80ml.99

Normal100 :- Total acid- 10 to 50 cu or degrees or m.Eq/L

Average:- 30 cu or degrees or m. Eq/L

Free acid101 :- It is defined as the amount of standard alkali

required to titrate 100ml. of Gastric juice up to PH 35. Normally in

fasting sample it is only 10-20ml. It increases & reaches with a

peak value one hour after the test meal. It remains high for half an

hour. The acid level comes back to the resting level within 3 hours.

Normal102 :- Free HCI 0 to 30 cu. Or degrees & m. Eq/L

Average - 18.5cu or degrees or m. Eq/L

Combined acidity103:- The portion between total acidity & free

acidity curves indicate combined acidity.

88  

Example:- For 10 ml of the gastic juice 3.2 ml. of 0.1 N NaOH

required with the Tofers indicator & 3.9 ml. (including 3.2 ml of the

first 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/L

Combined

acidity

- 39-32=7ml.

7x3.65=25.55 mg. HCI

i.e.7Eq/L

Gastric Analysis Test Limitaions:- A properly performed gastric

analysis requires a relatively large investment of time by the

physician who must perform the intubion & supervise the collection

of specimen. Although the procedure is begin experience, intubation

is apt to be unpleasant & sometimes traumatic for the patients. In

view of these facts and the inherent limitations of the information

gain through Gastric analysis. It is performed infrequently at the

present time. Gastroscopy, Roentgenography & Gastric cytology are

for more useful in establishing the diagnosis of Gastric pathology

than in gastric analysis.

89  

Drakshya

Raisin

90  

Haritaki

Hirda

Sharkara

91  

DRUG REVIEW

The Ayurveda believes in maintaining the balance of Tridosha

in the body to keep person healthy. The effect of certain Ayurvedic

preparations with the concerned vyadhihara Dravyas has been

explained with their therapeutic literature.

The pharmaco-dynamics of these drugs & their compound

preparation has been explained on the basis of Rasa, Guna, Virya,

Vipaka & Prabhava. An Ayurveda drug or diet or diet articles that

reverse or break the samprapti without producing any side effect

has been looked upon as ideal drugs or diets.

It has been well said by Acharya Charaka a drug that is not

understood perfectly is comparable to poision weapons, fire and the

thunderbolt-while the perfectly understood drug is comparable to

ambrosia.

The word drug is derived from the French work ‘Drogue’ which

means dry herb, drug as defined by who is a substance or product

that is used or intended to be used to modify or explore the

physiological systems or pathological states for the benefits of the

recipient.

The best drug is that which cures the disease promptly & also

preserve or sustains the health of an individuals.

It is the single active chemical entity present in a medicine

that is used for diagnosis in a medicine that is used for diagnosis

prevention treatment cure of a disease104.

92  

The drug which are having Tikta & Madhura – rasa, sheeta

virya & vatu-Vipaka Laghu & Ruksha property.

On the basis of above description ‘Drakshadi Gutika’ was

selected of its contents are having following property.

DRAKSHYADI GUTIKA

Reference : Bharat Bheshajya Ratnakara

It 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 the

reference.

The pts. Were advised for 2 gm TDS. After meal (1 tab will be

of 1 gm) sheetal jala as Anupana.

The chief properties & pharmacological action of the total

drugs under trial in the present study alongwith their probable

action on samprapti of the disease Amlapitta & other relevant

information as discussed below.

The detail of contents of Drakshyadi Gutika has been

described further.

Drug

Name

Rasa Virya Vipaka Guna Karma

Drakshya Madura Sheeta Madhura Singdha

Guru

Mridu

Vatta-pitta

Shamaka

Haritaki Except

Lavana

Ushna Madhura Laghu

Ruksha

tridoshahara

Sita Madhura Sheeta Madhura Guru

Snigdha

Vatta-pitta

Shamaka

93  

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 : Madhura

Guna : shigdha, Guru, Mridu.

Virya : Sheeta

Vipaka : Madhura

Doshaghnata : Vatapittashamaka

Chemical constituents :

Fruits contain grape-sugar (Glucose) gum, tanin, tartaric

citric, racemic & malic acids, chlorides of potassium & sodium,

94  

Sulphate of potash, tartrate of lime, magnesia, alum, iron some

albumin. Ozotised matters and acid tartrate of potassium.

Tartaric acid is the characteristic acid of the grapes. As o.05

mg. in 100 ccm in fruit-juice and oxalic acid in unripe fruits Raisins

contain calcium, magnesium, potassium, phosphorus and iron in an

assimilable form besides gum & sugar seeds contain a dense fixed

oil or fat & tannic acid 5 p.c. skins contain tanin. Wine contains from

7 to 24% of alcohol.

Pharmacological Activities :

Antifungal, angiotensin, converting enzyme (ACE) activity,

tumour inhibitory, Antiulcer, Hepatoprotective, antioxidant, wound

healing antimultagenic, antiherpetic, cardioprotective breast cancer

suppressor, antibacterial.

Actions & Uses :

The fruits are sweet refrigerant, laxative, demulcent intellect

promoting cardiotonic, haematinic, haemostatic diuretic aphrodisiac,

rejuvenating nervine tonic, febrifuge depurative, antispasmodic,

digestive, stomachic suppurative expectorant & tonic. They are

useful in burning sensation, dipsia, constipation, amentia, cardial,

debility, haemoptysis, haemorrhages, anaemia strangury,

consumptions & wasting diseases, fever, leprosy, skin diseases

dyspepsia, colic flatulence, cough, asthma, bronchitis, affections

of eyes and throat Bright’s disease, gout. Jaundice, & general

debility. The leaves are astringent anodyne, diuretic, depurative and

useful in cephalalgia strangury, scabies skin disease, syphilis,

haemorrhoids diarrhea, splenamegaly & vomiting the ash of the

stem is good for arthralgia vesical calculi, haemorrhoids & arehitis.

Sap young branches is used in skin diseases. The flowers are

95  

expectorant. Emmenagogue & haematinic & are useful in bronchitis,

liver disorders, anaemia, amenorrhoea & dysmenorrhoea.

2. HARITAKI

Botanical name : Terminalia Chebula

Natural order/family : Combrataceae

Synonyms : Haritaki, Abhaya, Pathya, Putana, Haimavati, Chetaki,

Shiva, Rohini.

Vernacular names :

English : Chebulik myrobalan

Hindi : Harad, pile-har, Hara.

Gujrati: Hardo.

Bengali : Haritaki

Marathi : Hirda, Hirda-phula, Bala hirade.

Part used : Fruit

Gana :

Prajasthapana, Jwaraghana (Ch.) Triphala, Amlakyadi, Parushakadi

(Su.)

Rasapanchaka (Pharmacodynamics) :

Rasa : Kashaya, Tikta, Madhura, Katu. Amla.

Guna : Laghu, Ruksha.

Virya : Ushna

Vipaka : Madhura

Prabhava : Tridoshashamaka

Doshaghnata : Tridoshashamaka

96  

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 gm

Chemical Constituents :

Anthraquinone glycoside, Chebulic acid chebulagic acid, tunic

acid terchebin, tetrachebulin, Vitamin C (fruits), arachidic, behenic

linoteic, oleic, palmitic & stearic acids (fruit hernels), Chebulin

(flowers). 2 hydroxymicro meric acid, maslinic acid & 2 hydroxy

ursolic acid (leaves).

Pharmacological Activities :

Antimicrobial, antifungal, Antibacterial antistress,

antispasmodic, hypotensive, indurance, promoting activity, anti

hepatitis B virus activity, hypolipidaemic, inhibitory activity against

HIV-1 protease, anthelmintic; purgative.

97  

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, skin

diseases, leprosy stomatitis, hyperacidity & associated gastric

disorder, anorexia, indigestion, flafulence, constipation,

haemorrhoids. Jaundice hepato-splenomegaly, other abdominal

diseases, helminthiasis, anaemia, delirium, pharyngitis, hiccough,

dyspnoea, cough, coryza, asthma, scrotal, enlargement, urinary

disorders, vesical & renal calculi, soft chancre, seminal defects,

cephalagia, narcosis, fainting, epilepsy, ophthalmic diseases,

intermittent, fevers, cardiae disorders filoria, obesity, neuropathy

rheumatoid arthritis, whitlow, dandruff, general debility.

In combination & phyllanthus emblica & Terminalia bellirica

under the name Triphala fruits of Terminalia chebula are extensively

used as adjunct to other medicines in almost all diseases.

3.Sita (Khand Sharkara)105

Synonyms SHARKARA

Ayurvedic 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 Raktaja

roga.

98  

PLACEBO

Placebo is a Latin term which means, “I may please you.” The

placebo effect is an effect attributable to a medicament as a

procedure & is not due to any specific pharmacodynamic property of

the substance for the condition being treated. Placebo effect may be

defined as “how the patient’s perception of treatment influences

his/her response.”106.

This is an inert substance which is given in the garb of a

medicine. It works by psychological rather than pharmacological

means & often produces responses equivalent to the active drug

some individuals are more suggestible & easily respond to a

placebo- ‘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 not

require an active drug placebo is a Latin word meaning. I shall

please. 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 can

relaease, endorphins in brain-causing analgesia. Naloxone an opiod

antagonist, blocks. Placebo analgesia placebo effects can thus

supplement.

Pharmacological effects. However placebo effects are highly

variable even in the same individual e.g. a placebo may induce

sleep on the first night but not subsequently. Thus it has overy

limited role in practical therapeatics substances commonly used as

placebo are lactose tablets/ capsules & distilled water injection107.

99  

As therapeutic agents that work psychologically.

A placebo preparation is usually an inert substance like starch

or lactose A supportive physician-patient relationship generally is

preferable to the use of a placebo for promoting therapeutic

benefits Relief or lack of relief of symptoms upon administration of a

placebo is not a reliable basis for determining whether the

symptoms have a “psychogenic” or “somatic” origin.

Placebos can often produce relief of subjective symptoms

associated with psychological disturbances. This includes relief from

anxiety, headache, pain, insomnia, & breathlessness. Hence

pacebosare often employed in the treatment of certain diseases

where the psychic element is suspected to be responsible for

subjective symptoms objective responses such as increase or

decrease in neutrophills In eosinophils may sometimes be seen with

placebos.

When administered for its therapeutic effects the placebo

preparation.

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 be

shown by some sings such as strong taste, a colorful capsule or a

table of odd shape & sometimes even by obvious but harmless side

effect like coloured urine.

During clinical trials, placebos are used to eliminate the effect

of bias of the physician & patient, particularly in evaluating a new

drug claimed to be effective in conditions like bronchial asthma,

angina pectoris, and pain & psychiatric disorders. In such cases the

100  

placebo should be indistinguishable form the active medicament in

physical properties like colour, smell taste & form.

Placebo effect may be modified by:-

Personality of the physician-Reassurance & optimistic outlook

offer achieve a better effect. “The doctor himself must inspire

confidence. It is difficult to define this quality. It does not lie so

much in what is said as in the doctor’s shape & bearing & in those

instinetive signs whereby one animal unknowingly conveys its mood

to another.

Some have it & some do not. In this respect the hospital

specialist is an easier postion than the GPbecause he is backed by a

temple of healing which is cleary nearer the seat of power than a

wayside shrine. Since few doctors are good enough actors to

simulate the confidence they do not have it often happens that one

who is kind & credulous is a better healer than another who is

informed and critical placebo reactions go faster when both parties

have faith & in this respect knowledge is an inhibitor. It follows that

anyone who wants to know whether a cure was due to a drug and

therefore reproducible would have to observe the ceremony

conducted 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 nature

are not likely to benefit from placebos. Such negative reactors, on

the contrary, may become. Worse as per their own expectations. A

101  

strong negative reactor may even take a pride in saying that he or

she is “allergic to all drugs”.

Form of administration: it is not surprising that the greatest

placebo effect (as high as 81.7) is achieve with injections. This may

perhaps explain the preference for the use of injections by the

practitioners colour, taste presence or absence of stress are there

factors which modify placebo effect.

Like active drugs, placebos can produce certain adverse.

Subjective reaction such as drowsiness, headache, dryness of

mouth, fatigue, insomnia, constipation, impotence, difficulty in

concentrating & impotence, difficulty in concerntrating & a

“drugged feeling”. An abstinence syndrome which responds to

injection of normal saline, has been describe after prolonged

placebo therapy.

Much of the routine treatment such as vitamins,

tranquiliollisers & tonics prescribed by the doctors often acts as a

placebo for themselves too many phycians cannot “bear to think

they are doing nothing, so they like their patients are willing to

believe. They persuade themselves or are persuaded of the virtues

of their treatment.

Interpretation of clinical results:

After the completion of the clinical trial, the results are

subjected to statistical analysis If the difference between the two

groups of treatment is so large that the probability of its occurrence

simply by chance is less than 5 times in 100 (P<0.05), then the

new drug is said to have produced a significant effect. It is

necessary, however, to rule out all other possible explanations ofr

such difference, before the verdict is accepted.

Various statistical designs have been suggested to ensure that

the results obtained are as precise as possible without much

interference by other biological factors & individual bias & their is no

102  

doubt that such statistical safeguards are essential. However

elaborate statistic cannot validate a poorly designed and executed

clinical trial further, in a given study it is more important to know

whether a new drug is significantly better than the older one or

placebo in terms of its “clinical effect” & not merely statistically. In

fact, on effect whose reality is revealed only after elaborate

statistics is hardly likely to be clinically important.

“Statistical significance” & therapeutic significance” of results

are not necessarily equivalent. Many times statistics would show ‘a

statistically significant difference’ but is cannot tell whether such

difference really matters in therapeutics. Thus, drug may lower the

plasma cholesterol concentration statistically but may not prevent

cardiac infarction.

Most of the new drugs are not ‘wonder drugs’ & need proper

clinical assessment. Unfortunately, because of various factors the

quality of many clinical trials is for from satisfactory As pointed out

by the lancet, there is no doubt that a prior design of the trial is

important but “It is clearly not worth devoting such energy to trial

dasing.

If the trained observer is not both trained and observing.

After all, the controlled trial requires as much in ‘clinical

observation’ as it does in design No. one should play at clinical

trials” .

As pointed out by park house, “A good trial of a poor drug is a

great deal better than no trial at all . It is infinitely better than a

poor trial of a poor drug.” Event the use of double blind technique

does not guarantee valid. Results in an otherwise poorly designed &

executed study.

103  

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 & Adhoga

Amlapitta can be misdiagnosed as Chaardi & Atisara respectively.

These disease are caused due to Pittolvana Sannipata with

Avarna of vata Ushna. Tikshna, Katu, Amla, Guna of pitta Guru

Sheeta manda Guna of Kapha & Chala Ruksha Guna of vata is

mainly involved. The Avarana of vata should be considered. The

Rakta which is also There as dushya & which seems to be mainly

responsible for progression of Amlapitta & its complication must be

considered while formulating the treatment. Sangraha Granthakaras

have explained the line of treatment mainly divided into two

headings viz. shodhana & shamana.

In shaman chikitsa drugs should have Tikta & Madhura rasa.

Hence for the present study “Drakshyadi Gutika” is chosen as

shamana theorapy to eradicats the disease from root. & previous

studies have shown that no one has worked on this topic.

104  

Materials & Methods Clinical trial

Design

A prospective randomized open label controlled clinical trial

conducted on diagnosed patients.

Selection of the subject :

The pts of Amlapitta roga attending the OPD & IPD of the

hospital were selected. 60 pts. Fulfilling the diagnostic criteria were

selected for the present study. Pts. Were drown by random

sampling technique, irrespective of sex, cast religion & occupation,

they were advised to visit the hospital every week for regular check

up & to asses the effect of therapy there by If any patient leaves

the treatment without completing 30 days it will be decleared as

dropped 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)

105  

B) Exclusion Criteria

The patient with following types of known cases were excluded from

study.

a) Gastric ulcer/peptic ulcer.

b) Pregnancy

c) Gastric carcinoma

d) Esophageal varises

e) Haematemasis

f) Other malignancy

g) ZE syndrome.

Objective Criteria

Investigation

a) Gastric function test :

Free HCL between 25-50 ME q/L & total acidity between 50-70

mEq/L was considered for pt. study.

b) Laboratory Investigation :

Hb%

Urine complete

Stool (routine) for occult blood.

PLAN OF STUDY

Criteria for diagnosis :

A special proforma was prepared in corporating important

signs & symptoms of the diseases. At the onset a detailed clinical

history was taken & complete physical examination of each patient

was done on the basis of proforma other necessary investigations

were carried out to exclude other pathologies as well as for the

assessment of present health status of patients.

106  

MANAGEMENT OF THE PATIENTS :

Group – A :

Patients were treated with “Drakshyadi Gutika.”

Group – B :

Patients were treated with cap. Placebo.

a) Group – A

In this Group 30 pts. Were selected

Dose : 2 gm (1 tab. of 1 gm).

Kala : TDS (After meal).

Anupan : Sheetal jala

Duration : 30 days.

b) Group B :

In this group 30 pt. were selected

Dose : 1 cap

Kala : BD (After meal).

Anupan : Sheetal jala

Duration : 30 days.

Diet :

As the disease is directly connected diet & dietary habits, so

patient himself knows most of the things which exacerbates the

disease hence he tries to avoid those things. But a detailed

explanation regarding the Astavidha Ahara Ayatana & Ashna.

Pravicharas was given to all patients & requested them to follow the

same. However, they were asked to avoid too hot, oily, sour, spicy

for fatty food.

CONSENT :

Written consent of patient was taken before treatment.

107  

CRITETERIA FOR ASSESSMENT

Subjective Criteria

General symptoms score :

Gradation of symptoms.

0 1 2 3

No 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

108  

E) SHIRSHUL

a) Shirshul on fasting 3

b) Shirshul relieved by antacid 2

c) Shirshul with meal 1

d) No shirashul at all 0

Objective 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.

109  

OBSERVATION

In this clinical study of Amlapitta total 60 patients were

registered & categorized into two equal groups. In group A

(Drakshyadi Gutika) 30 patients were registered & 30 patients were

registered in group B (placebo) each patients of both groups

observed throughly and noted neatly.

The observations quoted from here onwards include data of

60 registered patients. The observations are analyzed in the form of

chart & graph.

Table No. 1

Age wise

Number of patients Age group

(in yr.) Group A Group B Total Percentage

20-30 15 20 35 58.33

31-40 8 6 14 23.33

41-50 5 2 7 11.66

51-60 2 2 4 6.66

The table 1 shows the age wise distribution of the sample

studied. It was found that 58.33 % the patients were from 20-30

yrs. 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. & only

6.66 % patients belonged to the age group of 51-60 yrs. Age.

110  

Table no. 2

Sex wise

Number of

patients Sex

Group A Group B

Total Percentage

Male 20 16 36 60

Female 10 14 24 40

Present statistical data as shown in table 2 reveals that

maximum i.e. 60 % of patients were males and remaining 40 % of

patients were females.

Table No. 3

Religion wise

Number of

patients Religion

Group A Group B

Total Percentage

Hindu 24 25 49 81.66

Muslim 2 1 3 5

Buddha 4 4 8 13.33

Table 3 shows that 49 patients (81.66 %) were Hindus, 3

patients (5 %) were from Muslim & 8 patients (13.33 %) were

Buddha community.

111  

Table No. 4

Marital status

Number of

patients Marital

status Group A Group B

Total Percentage

Married 23 22 45 75

Unmarried 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. 5

Educational status

Number of

patients Educational

Status Group A Group B

Total Percentage

%

Primary 7 6 13 21.66

Secondary 10 12 22 36.66

Graduate 12 11 23 38.33

Illiterate 1 1 2 3.33

It was found that 23 patients (38.33 %) were educated up to

Graduate, 22 patients (36.66 %) were educated upto Secondary, 13

patients (21.66 %) were educated upto primary level & only 2

patients (3.33 %) were Illiterate.

112  

Table No. 6

Occupation wise

Number of

patients Occupation

Group A Group B

Total Percentage

Labour 6 6 12 12

House wife 6 8 14 23.33

Service 12 9 21 35

Student 5 6 11 18.33

Farmer 1 1 2 3.33

It was observed that maximum no. of patients 21 patients (35

%) were servicemen/women, 14 patients (23.33 %) were

Housewives, 12 patients (20 %) were labours, 11 patients (18.33

%) were students & 2 patients (3.33 %) were farmer.

Table No. 7

Diet wise

Number of

patients Diet wise

Group A Group B

Total Percentage

Vegetarian 9 13 22 36.66

Mix 21 17 38 63.33

Table No. 7 reflects the dietary habits of the patients which

indicates that 38 patients (63.33 %) had mixed dietary habit & 22

patients (36.66 %) were vegetarians.

113  

Table No. 8

Prakruti wise

Number of

patients Prakruti

Group A Group B

Total Percentage

Vata-pitta 16 15 31 51.66

Pitta-kapha 5 8 13 21.66

Vata-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-pitta

prakruti, 16 patients (26.66 %) were having vata kapha prakruti &

13 patients (21.66 %) were having pitta-kapha prukruti.

Table No. 9

Vyasana wise

Number of

patients Vyasana

Group A Group B

Total Percentage

Alcohol 8 7 15 25

Tea 9 8 17 28.33

Coffee 3 2 5 8.33

Tobacco 5 5 10 16.66

Smoking 5 8 13 21.66

Table 9 shows maximum No. of patients 17 (28.33 %) were

having vyasana of Tea, 15 patients (25 %) were having the vyasana

of Alcohol, 13 patients (21.66 %) were having the vyasana of

Smoking, 10 patients (16.66 %) were having Tobacco chewers &

also 5 patients (8.33 %) were having vyasana of Coffee.

114  

Table No. 10

Economical wise

Number of

patients Economical

Group A Group B

Total Percentage

Higher Class 9 8 17 28.33

Middle Class 12 15 27 45

Lower Class 9 7 16 26.6

The data shown in table 10 suggest that majority i.e. 27

patients (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. 11

Agni wise

Number of

patients Agni

Group A Group B

Total Percentage

Sama - - - -

Vishama 7 4 11 18.33

Manda 19 21 40 66.66

Tikshana 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 having

Vishamagni, 9 patients (15 %) were having Tikshnagni & no.

patients was having Samagni.

115  

Table No. 12

Koshtha wise

Number of

patients Koshtha

Group A Group B

Total Percentage

Madhyama 16 17 33 55

Krura 5 3 8 13.33

Mrudu 9 10 19 31.66

This table highlights the Koshtha wise distribution of the

sample studied, 33 patients (55 %) were having Madhyama

Koshtha & 19 patients (31.66 %) were having Mrudu koshtha, while

8 patients (13.33 %) were having Krura Koshtha.

Table No. 13

Satva wise

Number of

patients Satva

Group A Group B

Total Percentage

Pravara 7 5 12 20

Madhyama 13 14 27 45

Avara 10 11 21 35

Table no. 13 shows that maximum no. of patients i.e. 27

patients (45 %) were having Madhyama satva, 21 patients (35 %)

were having Avara Satva, while 12 patients (20 %) were having

Pravara satva.

116  

Table No. 14

Satmya wise

Number of

patients Satmya

wise Group A Group B

Total Percentage

Pravara 9 10 19 31.66

Madhyama 17 15 32 53.33

Avara 4 5 9 15

Table no. 14 shows 32 patients (53.33 %) were having

Madhyama Satmya, 21 patients (31.66 %) were having Pravara

Satmya & only 9 patients (15 %) were having Avara Satmya.

Table No. 15

Sarata wise

Number of

patients Sarata

Group A Group B

Total Percentage

Pravara 6 6 12 20

Madhyama 21 22 43 71.67

Avara 3 2 5 8.33

Table no. 15 shows Sarata wise distribution of the patients in

this series maximum no. of 43 patients (71.67 %) were having

Madhyama Sarata, 12 patients (20 %) were having Pravara Sarata

& only 5 patients (8.33 %) were having Avara Sarata.

117  

Table No. 16

Samhnana wise

Number of

patients Samhnana

Group A Group B

Total Percentage

Pravara 8 8 16 26.66

Madhyama 21 19 40 66.66

Avara 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 %) were

having Avara Samhnana.

Table No. 17

Dominance of Rasa wise

Number of

patients Dominance

of Rasa Group A Group B

Total Percentage

Madhura 5 3 8 13.33

Amla 5 6 11 18.33

Lavana 4 3 7 11.66

Katu 10 11 21 35

Tikta 3 4 7 11.66

Kashaya 3 3 6 10

Maximum no. of patients i.e. 21 patients (35 %) were having

Katu rasa pradhana Ahara, 11 patients (18.33 %) were having Amla

rasa pradhana Ahara, 8 patients (13.33 %) were having madhuru

rasa prdhana Ahara, 7 patients (11.66 %) were having Lavana rasa

as well as 7 patients (11.66 %) were having Tikta rasa & and only 6

patients (10 %) were having kashaya rasa pradhana Ahara.

118  

Table No. 18

Amlapitta Bheda wise

Number of

patients Amlapitta

Bheda Group A Group B

Total Percentage

Vataja 4 6 10 16.66

Pittaja 18 17 35 58.33

Kaphaja 8 7 15 25

Table no. 18 shows 35 patients (58.33 %) were having pittaja

Amlapitta, 15 patients (25 %) were having kaphaja Amlapitta &

only 10 patients (16.66 %) were having vataja Amlapitta.

Table No. 19

Predominant Manasa Bhava wise

Number of

patients

Predominant

Manasa

Bhava Group A Group B

Total Percentage

Chinta 18 19 37 61.66

Krodha 13 13 26 43.33

Shoka 3 7 10 16.66

Bhaya 6 5 11 18.33

None 3 3 6 10

As the data reveals that 37 patients (61.66 %) were having

Chinta, 26 patients (43.33 %) were having Krodha as predominant

manasa bhavas, 11 patients (18.33 %) were having Bhaya, 10

patients (16.66 %) were having shoka.

119  

Table No. 20

Ahara Shakti wise

Number of patients Shakti

Group A Group B Total Percentage

Abhyavaharana

Shakti

Parvara 2 3 5 8.33

Madhyama 10 12 22 36.66

Avara 18 15 33 55

Jarana shakti

Pravara 1 2 3 5

Madhyama 20 16 36 60

Avara 9 12 21 35

Maximum number of patients i.e. 55 % were having avara

Abhyavaharana Shakti while 36.66 % were having madhyama

Abhyava harana shakti & 8.33 % were having Pravara

Abhyavaharana Shakti.

60 % patients were having Madhyama jarana Shakti while 35

% patients were having avara & 5 % patients were having Pravara

Jarana Shakti.

Table No. 21

Sleeping Pattern wise

Number of

patients Nidra

Group A Group B

Total Percentage

Alpa 4 3 7 11.66

Samayaka 19 20 39 65

Khandit 5 4 9 15

Prabhut 2 3 5 8.33

120  

The above table shows that maximum no. of patients 65 %

were having Samayaka Nidra, 15 % patients were having Khandit

Nidra, 11.66 % patients were Alpa Nidra & only 8.33 % patients

were having prabhut Nidra.

Table No. 22

Subjective Criteria wise

Group A Group B

BT AT BT AT

Complaints

No. of

Pts

% No.

of

Pts

% No.

of

Pts

% No.

of

Pts

%

Avipaka 30 100 19 63.33 29 96.66 30 100

Tikta

Amlodgara

17 56.66 5 16.66 24 80 21 70

Hrud Kanta

Daha

28 98.33 16 53.33 25 83.33 28 93.33

Chardi 16 53.33 8 26.66 14 46.66 11 36.66

Shirashula 17 56.66 9 30 27 90 27 90

01. In Group A Before treatment Avipaka was found in 30 patients

(100 %) while After treatment Avipaka is reduced & found in 19

patients (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 17

patients (56.66%) but After treatment it reduced & found in 5

patients (16.66 %)

In Group B Before treatment Tikta Amlodgara was found in 24

patients (80.00%) but After treatment it reduced & found in 21

patients (70 %)

121  

03. In Group A Before treatment Hrud Kanta Daha was found in 28

patients (98.33%) while After treatment it reduced in 16 patients

(53.33 %)

In Group B Before treatment Hrud Kanta Daha was found in

25 patients (83.33%) while After treatment it reduced in 28

patients (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 27

patients (90%) while After treatment it reduced in 27 patients

(90%)

Table No. 23

Objective Criteria wise

Group A Group B Criteria

BT AT BT AT

Mean Free

HCL

22.23 19.52 20.28 20.1

Mean Total

Acid

32.55 30.83 32.27 32.06

01. In Group A Before treatment Mean Free HCL was found in 22.23

while After treatment it reduced in 19.52

122  

In Group B Before treatment Mean Free HCL was found in

20.28 while After treatment it reduced in 20.1.

02. In Group A Before treatment Mean Total Acid was found in

32.55 while After treatment it reduced in 30.83

In Group B Before treatment Mean Total Acid was found in

32.27 while After treatment it reduced in 32.06

123  

No

.of

Pati

en

ts

Graph No.1 : Distribution of Patients according to Age

No

.of

Pati

en

ts

Graph No.2 : Distribution of Patients according to Sex

No

.of

Pati

en

ts

Graph No. 3 : Distribution of Patients according to Religion.

124  

No

.of

Pati

en

ts

Graph No. 4 : Distribution of Patients according to Marital Status.

No

.of

Pati

en

ts

Graph No. 5 : Distribution of Patients according to Educational Status.

No

.of

Pati

en

ts

Graph No. 6 : Distribution of Patients according to Occupation.

125  

No

.of

Pati

en

ts

Graph No. 7 : Distribution of Patients according to Diet.

No

.of

Pati

en

ts

Graph No. 8 : Distribution of Patients according to Prakruti.

No

.of

Pati

en

ts

Graph No.9 : Distribution of Patients according to Vyasana.

126  

No

.of

Pati

en

ts

Graph No.10 : Distribution of Patients according to Economical Status.

No

.of

Pati

en

ts

Graph No.11 : Distribution of Patients according to Agni.

No

.of

Pati

en

ts

Graph No.12 : Distribution of Patients according to Koshta.

127  

No

.of

Pati

en

ts

Graph No.13 : Distribution of Patients according to Satva.

No

.of

Pati

en

ts

Graph No.14 : Distribution of Patients according to Satmya.

No

.of

Pati

en

ts

Graph No.15 : Distribution of Patients according to Sarata.

128  

N

o.o

f P

ati

en

ts

Graph No.16 : Distribution of Patients according to Samhana.

No

.of

Pati

en

ts

Graph No.17 : Distribution of Patients according to Dominance of Rasa.

No

.of

Pati

en

ts

Graph No.18 : Distribution of Patients according to Type of Amlapitta.

129  

No

.of

Pati

en

ts

Graph No.19 : Distribution of Patients according to Manas Bhava.

No

.of

Pati

en

ts

Graph No.20 : Distribution of Patients according to Abhyaran Shakti.

No

.of

Pati

en

ts

Graph No.20 B : Distribution of Patients according to Jarana Shakti

130  

No

.of

Pati

en

ts

Graph No.21 : Distribution of Patients according to Sleeping Pattern.

No

.of

Pati

en

ts

Graph No.22 : Distribution of Patients according to subjective criteria.

No

.of

Pati

en

ts

Graph No.23 : Distribution of Patients according to objective criteria.

131  

RESULTS

Effect of therapies:

Total 60 patients were registered for treatment all 60 patients

were completed the course of whole treatment, 30 patients in

Group A, 30 patients in Group B. effect of Therapies on treated 60

patients and the results of 60 being present here.

Table No. 24

Avipaka:

Mean

Group BT AT

X

S.D. S.E. t P

Group A 1.87 0.77 1.10 0.75 0.14 8.07 P<0.01

Group 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 of

Avipaka, before treatment was 1.87 which reduced to 0.77. The

reduction occurred is statistically significant which means

Drakshyadi 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 placebo

is not effective.

132  

Table No.25

Tikta- Amlodgara.

Mean

Group BT AT

X

S.D. S.E. t P

Group A 0.77 0.17 0.6 0.6 0.11 5.45 P<0.01

Group 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. The

reduction occurred is statistically significant which means

Drakshyadi 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 showing

placebo is not effective.

Table No. 26.

Hrud Kantha Daha:

Mean

Group BT AT

X

S.D. S.E. t P

Group A 1.5 0.6 0.9 0.8 0.15 6 P<0.01

Group 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 Hrud

Kantha Daha, before treatment was 1.5 which reduced to 0.6. The

reduction occurred is statistically significant which means

Drakshyadi Gutika is effective for Hrud Kantha Daha.

133  

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 showing

placebo is not effective.

Table No. 27.

Chardi

Mean Group

BT AT

X S.D. S.E. t P

Group A 0.87 0.27 0.6 0.72 0.13 4.61 P<0.01

Group 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 of

Chardi, before treatment was 0.87 which reduced to 0.27. The

reduction occurred is statistically significant which means

Drakshyadi Gutika is effective for Chardi.

While in Group B, the mean value of Chardi, before

treatment was 0.7 which reduced to 0.57 after treatment. The

reduction occurred is statistically not significant showing placebo is

not effective.

Table No. 28

Shirashula:

Mean Group

BT AT

X

S.D. S.E. t P

Group A 0.9 0.3 0.6 0.72 0.13 4.61 P<0.01

Group 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 of

Shirashula, before treatment was 0.9 which reduced to 0.3. The

134  

reduction occurred is statistically significant which means

Drakshyadi Gutika is effective for Shirashula.

While in Group B, the mean value of Shirashula, before

treatment was 1.3 which reduced to 1.233 after treatment. The

reduction occurred is statistically not significant showing placebo is

not effective.

Table No. 29

Free HCL

Mean Group

BT AT

X S.D. S.E. t P

Group A 22.23 19.52 2.71 1.92 0.35 7.77 P<0.01

Group 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 Free

HCL, before treatment was 22.23 which reduced to 19.52. The

reduction occurred is statistically significant which means

Drakshyadi Gutika is effective for Free HCL.

While in Group B, the mean value of Free HCL, before

treatment was 20.28 which reduced to 20.1 after treatment. The

reduction occurred is statistically not significant showing placebo is

not effective.

Table No. 30

Total Acid

Mean Group

BT AT

X S.D. S.E. t P

Group A 32.55 30.83 1.72 1.04 0.19 9.05 P<0.01

Group B 32.27 32.06 0.18 0.59 0.11 1.64 P>0.01

135  

The above chart shows that in group A, mean value of Total

Acid, before treatment was 32.55 which reduced to 30.83. The

reduction occurred is statistically significant which means

Drakshyadi Gutika is effective for Total Acid.

While in Group B, the mean value of Total Acid, before

treatment was 32.27 which reduced to 32.06 after treatment. The

reduction occurred is statistically not significant showing placebo is

not effective.

Overall effect of Drakshyadi Gutika on 30 paitents of

Amlapitta

Result Group A Group B

No. of

patients

% No. of

patients

%

Cured 12 40 0 0

Improve 15 50 0 0

Unchange 3 10 30 100

(Chi-Square Value) 2

= 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 unchange

result.

In group B, out of 30 patients neither a single patient cured

nor improved. All 30 patients showed unchanged result.

It means Drakshyadi Gutika is highly effective remedy for

Amlapitta.

The chi-Square Value of above table is 37.02 which is highly

significant showing Drakshyadi Gutika, is highly effective in

Amlapitta.

136  

DISCUSSION Ayurvedic stand apart from the rest of medical fraternity with

its holistic approach to a patient as a conglomeration of mind, body

and spirit too. The first and foremost task in Ayurvedic disease

management is a proper understanding and description of its

etiopathogenesis. Acharya Vagbhata109 as well as Acharya

Charaka110 has clearly defined the role of Agni in the

etiopathogenesis of disease. In recent years there has been an

unprecedented increase of incidences related to GI system, due to

changes in life style, diet pattern, behavioural pattern etc,which

hamper the normal physiology of digestion/ Agni of body.

Amlapitta is a disease of Annavaha Srotas i.e. Amasaha

Samuttha which is mainly the seat for Agni. Any disturbance to Agni

caused due to irregular diet and behavioural pattern well as the

involvement of mental stress and strain, leads to the disease

Amlapitta.

In Samhita some words have also been mentioned in the

reference of Amlapitta. i.e. Jaratapitta seems as synonym for

Amlapitta. and Amlaka, Dhumaka, Vidaha, Amlika, Prameelaka,

Pitta Visuchika, Pittamala and Suktata, denotes the different aspects

of the abnormal state of Pitta. These are the major symptoms of

dyspeptic disease indicates towards Pittolvana condition.

Charaka Samhita is the first medical literature bears 9 places

reference regarding Amlapitta have been found. Though he has not

mentioned, Amlapitta as a separate disease entity, but from the

references. It gives a clear cut indication regarding the Nidanas,

Samprapti, and management in his period.

137  

Sushruta and Vagbhata have not at all mentioned the word

Amlapitta. Kashyap was the first person who described the disease

vividly and analyzed it on Doshik basis and give the importance of

its management. Madhavakara has described the disease

separately. Shrikanthadatta describes the disease by giving

different quotation. Latter workers of Sangrahakala followed the

same as Madhavakara and Kashyap.

Nidana: Kashyap and Madhavakara both have given the long list

of Nidanas of Amlapitta. They have different opinion regarding

etiopathological factors.

Kashyap has mentioned the Nidanas which represents the

involvement of Doshas (Vatadayh) i.e. Tridoshs. Where as

Madhavakara has mainly given Pitta aggravation factors responsible

for this. Manasika factors also have strong role in the Nidanas of

Amlapitta, as stated in Charaka111 that Ama production is also due

to the involvement of mental stress and strain which hamper the

normal digestion and metabolism. In present day situation it has

been proved beyond doubt that the Manasika Bhavas have their

direct impact on digestion and metabolism. Hence Manasika Bhavas

should be included in list of Amlapitta.

Shadavidha Aharabhava are very important in explaining the

physiology of digestion and pathology caused by Nidanas. These six

factors also greatly depend upon Ashtavidha Ahara Ayatana and

Dwadasasana Pravicharana. If looking according to Dosha functions

Ushna is depend upon Pitta, Vayu and Kala and Vata, Kleda and

Sneha on Kapha. So any disturbance in the diet qualities or process

may start the pathogenesis by disturbing the digestion process

directly (Agnidushti).

138  

In modern medicine, H. pylori takes a major role in the

production of disease Amlapitta.

Samprapti:

The pathogenesis of the diseases as per Ayurvedic concept

requires the three components i.e. Dosha, Dushya and Nidana. In

Amlapitta the Nidanas are predominantly from the non compliance

of dietetic code of selection and eating. However psychological

status of a person plays an important role.

While describing the Samprapti of Grahani Dosha Acharya

Charaka has mentioned the production of Amlapitta. According to

him when diet is improperly digested, it gets fermented and forms

Amavisha, when this Amavisha gets mixed with Pitta, it develops

the disease Amlapitta. Where as Kashyap believed that the disease

caused by vitiation of Doshas (Vatadaya) i.e. Tridosha causing

Mandagni leads to Vidagdhajirna manifesting as Amlapitta.

Madhavakara in the line of Charaka describes the

development of Amlapitta due to Pitta aggravating factors. Also

Kashyap considered Apakva Madya and Dugdha as causative

factors112 for the same and Acharya Charaka lists Dugdha as one of

the Pathya for Amlapitta.

Depending on the status of Nidanas either Kapha, Pitta or

Vata, the basic Samprapti of Amlapitta can be conceived from the

clues given by Charaka113, Kashyap, Madhavakara and also

Samprapti of Parinamashula describe by Madhavakara and

Vijayarakshita. Considering all Samprapties it can be conceived that

disease Amlapitta can occur by all the three Doshas. The main

consideration of the qualities concerned are Ushna, Tikshna, Katu,

139  

Amla and Sara Guna of Pitta, Guru, Shita, Manda Guna of Kapha

and Chala, Ruksha Guna of Vata.

So, Amlapitta is a condition where Amla Guna is increased

due to Samata causing Vataadi condition.

Looking to the status of chief Dosha at the site of Amlapitta

i.e. Pitta, most common route is the Pitta predominant which have

been consider by Charaka and subsequently by Madhavakara.

However second common route of Amlapitta, pathogenesis is Kapha

predominant which have been consider by Kashyap and further

supported by Vijayarakshita, while explaining the pathogenesis of

Parinamashula.

While explaining the pathogenesis of Amlapitta concept of

various Avaranas as explained by Charaka in Vatavyadhi should also

be taken into account. It may be Kaphapittavrita Vata. However

Avarana may be three types.

1. Samavata Avrita by Vriddhapitta and or Kapha

2. Vriddhavata Avrita by Samapitta and or Kapha

3. Vriddhavata Avrita by Vriddhapitta and or Kapha

In the disease Amlapitta third pathogenesis is rare. Hence

first two commonly encounter, which may give the clinical

conditions like Kapholvana and Pittolvana type of Amlapitta.

As Chakrapani explains that Urdhva Amashaya is the seat for

Kapha and Adhoamashaya is the seat for Pitta. And also there is

more chance of involvement of local factor in the pathogenesis

process. Hence Kapha and Pitta predominance should be

considered.

140  

Also Acharya Charaka has given various conditions which may

help in explaining the pathogenesis of Amlapitta. These are

Pittavritta Vata114, Pittavrita Prana115, Kaphavrita Prana116 and

Pittavrita Samana116.

The Samprapti of Gastro intestinal disorder constitutes the

different stages and each stage has been accepted as a separate

disease entity. Later on by various workers like Ajirna, Amlapitta,

Parinama Shula etc. Vidagdhajirna is the initial stage of Amlapitta

caused by vitiation of Pitta mainly Drava and Amlaguna.

Vidagdhajirna is an acute and aetiology dependent

disorders, where as Amlapitta is a chronic disorder and once

manifested then not dependent on Nidana. Vidagdhajirna is

precursor of Amlapitta and can be cured by Nidana Parivarjana only

or with addition of Langhana and this is the main difference

between two.

Due to the similarities in Sthanika Doshas and Adhisthana

diseases like Vidagdhajirna Paittika Grahani, Paittika Atisara,

Paittika Shula, Ammadrava Shula and Parinama Shula bears similar

symptomatologies and creates much confusion in diagnosis. A

carefully recorded history and Pratyatma ling of diseases may

waved out the suspicion in diagnosis.

Because of the above description resembles with Amlapitta,

great emphasis is given to disease by the research workers on

Ayurvedic medicine. All the later workers trying to correlated

Amlapitta with some modern disease entities such as gastritis,

Peptic ulcer, duodenal ulcer, hyper acidity, hyperchlorhydira and

also hypochlorhydria. Probably to confirm to one characteristic of

the entity namely its Bhishakamohakaratva or confusing nature.

141  

Many Researchers have brought out a new concept that Amlapitta is

not only hyperchlorhydria but the patients having both hyper as well

as hypochlorhydriya shows the same sign and symptoms of

Amlapitta. And they have concluded that Amlapitta is nothing but

gastritis syndrome. Their results were very encouraging and taken a

new approach towards the whole problem and thrown much light for

future research workers.

So, Gastritis refers to inflammation of the gastric mucosa,

which is not a single disease but rather a group of disorder, due to

intake of various irritant substances or endocrinal factors, due to

any reflexes or due to any bacterial, viral or fungal infection out of

these infection, H pylori is the most common ailments in the

pathogenesis of Gastritis.

Purvarupa: Purvarupa of disease is not mentioned in any classics.

But according to Shadvidhakriyakala, the stage of Sanchaya and

Prakopa may be considered as Purvarupa of disease.

Rupa: Madhavakara has given general symptoms of Amlapitta as

Avipaka, Klama, Utklesha, Tikta– Amla Udgara, Gaurava, Hrit–

Kantha Daha, Aruchi etc. Madhavakara has classified Amlapitta in

two types according to gati i.e. Urdhvaga and Adhoga Amlapitta

Adhoga variety cannot be diagnosed easily as mentioned by

Vangasena. It’s told that – there is very difficult to do differential

diagnosis between Adhoga Amlapitta, Paittika Grahani and Paittika

Atisara. Also he told that even the intelligent Vaidyas get very much

confused 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.

142  

Vatika, Vata Kaphaja, Kaphaja and Kapha Pittaja. Kashyap has

mentioned 3 types i.e. Vatolvana, Pittolvana and Kapholvana.

Urdhvaga variety of Amlapitta may be further classified as Doshika

predominant type.

Acharya Kashyap explained about Upashaya and Anupashaya

according to Doshik types. Amlapitta is considered as Sukhasadhya

in earlier stage and of short duration but later on becomes Krichhra

Sadhya, Yapya and becomes Asadhya when accompanied with

Upadravas. Upadravas has not been described by any ancient

Acharya except Kashyap and Gananatha Sen i.e. Jwara, Atisara,

Pandu etc. Acharya Kashyap and Charaka have mentioned that this

disease occurs mostly to the persons having Jihvalaulya. Hence

after some recovery the person again gets involved in Mithya Ahara

Vihara due to Jihvalaulya and the disease again gets provoked. This

vicious cycle goes on and the disease becomes chronic. Acharyas

have described various guideline principles for the management.

Among them, Nidana Parivarjana plays major role. Various

preventive measures are explained which helps in preventing as

well as development of Amlapitta. Treatment modality mainly

includes Shodhana and Shamana therapy. Among Shodhana,

Vamana and Virechana have been advised followed by Basti. In

Shamana therapy, Madhura, Tikta, Katu, Amla predominant Rasa

Sheeta, Ushna Virya drugs have been used. So, in the present study

‘Drakshyadi Gutika’ has been given patients having pitta

predominant Amlapitta, as it contains drugs having Madhura Sheeta

Virya and Guru, Snigdha property.

Amlapitta as its maximum drugs are having Katurasa, Laghu,

Ruksha property and Ushna Virya.

143  

Also Pathya-Aathya forms an important part of the treatment

in this disease. Patient has been advised to follow Dwadasha asana

Pravicharana and restrict the use of Amla, Lavana, Katu Rasa,

Ushna and Tikshna Guna diet according to their Doshika

predominance.

With an aims and objective to provide a better diagnostic and

therapeutic approach this study had been conducted. Patients

coming to our department O.P.D. or the diagnosed cases of

Amlapitta were properly examined on the basis of specially

prepared protocol and data recorded from the study are as follows

Age :-

Maximum no. of patients, i.e. 35 patients (58.33 %) were

belonging to 20-30 yrs. Age group followed by 14 patients (23.33

%) in 31-40 yr. this indicates that the middle aged populations are

affected by this disease more, which is pitta predominant period of

life. This pitta predominance makes disease chronic and krichhra

sadhya.

Further this age group are one for whom hurry, worry & curry

has been advised to be restricted. In this age group nobody is going

to restrict themselves for any dietetic and behavioural code. These

decades are most productive age of the human, hence everybody is

under stress to deliver more within short period.

Sex :-

Out of 60 patients; 36 patients (60 %) were male. This may

be due to faulty dietary habits, increased stress & strain among

males & also due to habits like smoking pan etc.

144  

Religion :-

Maximum 41 patients (81.66 %) patients were Hindu. The

hospital where study have been conducted is situated in Hindu

predominant area and most of the population coming to the hospital

belong to same community. So, it can not be concluded that Hindu

are 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 family

involved patients were under stress due to various reasons.

Educational status :-

In this study 23 patients (38.33 %) were educated this may

be because of fast life style, irregular food habits stressful condition

these reasons for the incidence of Amla pitta.

Occupations :-

21 patients (35 %) were service holder followed by 14

patients (23.33 %) were housewives. This incidence in service

holder, may be due to hurried & worried life irregular diet habits.

Etc. where as in housewives, may be under stress due to various

familiar reasons.

Diet :-

Maximum no. of patients i.e. 38 patients (63.33 %) were

mixed diet the reason may be excessive use of spicy food which

provak the pitta-kapha dosha presominantly.

Deha prakriti :-

Maximum 51.66 % (31 patients) were having vatta-pitta

prakriti while 26.66 % (16 patients) had vatta kapha prakriti.

145  

Vyasana :-

Maximum patients i.e. 17 patients (28.33 %) were used to

tea while 25 % (15 patients) were addicted to alcohol.

So this may impair Agni & favour for manifestation of

Amlapitta.

Social Economical status :-

27 patients (45 %) were from middle class & reason for this

may be untimely food intake increase family members in a

congested 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 the

root cause of Urdhwaga Amlapitta.

Koshtha :-

It is observed that Urdhwaga Amlapitta occurs is more in the

people having madhyama koshtha followed by Mrudu kostha.

Madhyama & Mrudu koshtha reflect the predominance of kapha &

pitta which are the main dosha involved in pathogenesis of

Urdhwaga 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.

146  

Dominance of Rasa :-

Maximum no. of patients 21 patients (35 %) were taking katu

rasa pradhana diet followed by 11 patients (18.33 %) were taking

Amla rasa pradhana diet excessive intake of these Rasas vitiates

Pitta & kapha which finally may lead to Amlapitta.

Ahara Shakti :-

33 patients (55%) were having avara Abhyavaharana Shakti

followed by 22 patients (36.66%) Madhyama Abhyavaharana

Shakti.

36 patients (60%) were having Madhyam Jarana Shakti

followed by 21 patients (35%) were having Avara Jarana Shakti.

The resion probably for this is, in this disease there is impairment of

Agni.

Sleeping habit :-

Majority of the patients were (65 %) having Samyaka Nidra

followed 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 followed

by 43.33% having Krodha which is responsible for improper

digestion leads to Ajirna like condition as mentioned in Ayurvedic

classics.

147  

Cordinal signs & Symptoms

As mentioned earlier in theclinical study, Avipaka was found in

98.33% Hrudkhanta Daha in 88.33%, Shirshula in 73.33% Tikta

amlodagara in 68.33% & Chardi 50%. As these were the cardinal

symptoms. It was expected to haved finding like this but the

quantum of these findings was important these findings may be due

to Amla/ Katu Pradhana Rasa diet or other faulty dietetic habits

mental condition sleeping pattern etc. the degree of Severity was

different 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 unchange

result.

In group B, out of 30 patients neither a single patient cured

nor improved. All 30 patients showed unchanged result.

It means Drakshyadi Gutika is highly effective remedy for

Amlapitta.

The chi-Square Value is 37.02 which is highly significant

showing Drakshyadi Gutika, is highly effective in Amlapitta.

148  

SUMMARY

The Dissertation entitled “To study the efficacy of

Drakshyadi 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 & Urdhwaga

Amlapitta, Aim & Objectives of the study.

In the Historical review, reference regarding the Amlapitta

diseases during different period of time viz. vedic period, samhita

kala were compied under the heading Historical Review of

Amlapitta.

Amla pitta – Ayurvedic view of which deals with Ayurvedic

concept of the diseases. Viz. Etymology Defination, Synonyms,

Classification, Aetiology, pathogenesis, premonitory, Symptom,

149  

Symptoms Exploratory, Symptoms, Complications, Prognosis,

Differential Diagnosis, Treatment, Pathya-Apathya.

Amlapitta – Modern review, the description of Amlapitta from

modern 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 of

H. 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, Research

methodology, controlled conditions & lastly criteria for assessment

of resuls.

Observations & Results – observation were made c regard to age,

sex etc. the results of the study were analyzed statistically and are

presented with discussion.

It also includes discussion about probable mode of action of

research drugs on Amlapitta.

Summary of contents of this dissertation have been mentioned.

Clonclusion drawn on the basis of present study have been

discussed and lastly references & Bibliography is included

respectively.

150  

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.

151  

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.

152  

ABBREVIATIONS

A. H. Ashtanga Hridaya

A. S. Ashtanga Sangraha

B. P. Bhavaprakasha

Bh. Bhela samhita

Ch. Charaka samhita

Ch. Su. Chark Sutrasthana

Ch. Chi. Charak Chikitsasthana

Chakra. Chakrapani

Ha. Sam. Harita samihita

Ka. Kashyapa smahita

Ka. Sam. Kashyapa samhita

M. N. Madhava Nidana

Ni. Nidansthana

Pu. Purva Khanda

Sha. Sharangadhara

Si. Siddhi sthana

Su. Sushruta samhita

Up. Uttartantra

Vi. Vimanasthana

Y. R. Yogaratnakara.

S.N. Siddhant Nidana

Ks. Khi. Kashyap Khilsthana

153  

REFERENCES

Introduction :

1. Ka.Khi. 7/12 5. Ka.Khi. 16/1

2. Ch.Chi. 15/3/4 6. M.Ni. 12/1

3. Ch.Chi. 15/44-49 7. API Medicine 7th Edition P.No.563

4. As.Hr.Ni. 12/1

Conceptual Study :

8. Ch.Chi. 15/3 20. Cha.Chi.15/42-44

9. Ch.Chi. 15/3 21. Ma.Ni. 51/2

10. Ch.Chi.15/15 22. Ch.Chi.15/9

11. Ch.Chi. 15/13 23. Ah.Su. 9/20

12. Ch.Chi.15/15 24. Su.Su. 21/13, Ah.Su. 12/17

13. Ch.Chi. 15/42 25. Cha.Chi.15/6

14. Ch.Chi.15/13 26. Cha.Chi. 15/6

15. Ch.Chi. 15/15 27. Cha.Chi.15/10

16. Ch.Chi.15/13 28. Cha.Chi. 5/11

17. Ch.Chi.15/13 29. Cha.Chi.15/11

18. Ch.Chi.15/13 30. Cha.Cha.6/14

19. Ch.Chi. 15/15 31. Su.Su. 21/9

32. Su.Su.25/27-28 34. Su.Su. 46/487-488

33. Su.Su. 21/16

Disease Review :

35. Ch.Chi. 15/3 40. Ch.Su. 27/25

36. Ch.Su. 20/14 41. Ch.Su. 7/148

37. Cha.Su.25/40 42. Ch.Su. 12/52

38. Ch.Su. 26/43 43. Ch.Chi. 15/47

39. Ch.Su. 26/103

154  

Ayurvedic Review :

44. Ah.S.Su.5/27 54. Su.Su. 35/35

45. Ah.S.Su.5/27 55. Ch.Su. 12/11, Su.Su. 21/9

46. Ah.S.Su.20/16 56. Ch.Chi. 15/45-60

47. Ma.Ni. 51/1 57. Si. Ni. Chi. 5

48. Ka.Khi.16, M.N.51/1 58. Ch.Su. 19/5, A.S. Su.22/10

49. Ka.Khi. 16/6 59. Ka.Khi. 16/18

50. Cha.Vi. 21/1 60. M.Ni. 51/7

51. Ka.Khi. 16/44 61. Kha.Khi. 16/99

52. Ka.Khi.16/45 62. A.S.Su. 24/8, A.H.Su. 14/6

53 M.Ni. 51/2 63. Ka.Khi. 16

Modern Review :

64. Textbook of Pathology – Harsmohan Pg. No. 519

65. Das – Ch. 44 pg.No. 814

66. Concise Medical Physiology Pg.No.79

67. Concise Medical Physiology Pg.No.79

68. Concise Medical Physiology Pg.No. 1597-1598

69. Essential of Med.Pharm. Triphati- Pg.No. 629-630

70. Textbook of med.Physiology Gyton & Hall Pg.No. 745

71. Textbook of Pathology by Harsshmohan Pg.No. 522

72. Clinical Med. Pg.No. 390

73. Textbook of Pathology by Harsshmohan Pg.No. 523

74. Clinical Med. Pg.No. 391

75. Clinical Med. Pg.No. 390

76. Medicine for Stud. Golwalla Pg. No.17

77. Medicine for Stud. Golwalla Pg. No.18

78. Text Book of Physiology Gyton & Hall Pg. No. 764

79. Textbook of Pathology by Harsshmohan Pg.No. 524

155  

80. Textbook of Pathology by Harsshmohan Pg.No. 524

81. Textbook of Pathology by Harsshmohan Pg.No. 524

82. Clinical Medicine Pg. No. 394

83. Basic Pathology by K.C.Robbin Pg. No. 484

84. Clinical Medicine Pg. No. 394

85. Clinical Medicine Pg. No. 393

86. Clinical Medicine Pg. No. 394-195

87. Medicine for Stud. Golwalla Pg. No.18

88. Textbook of Pathology by Harsshmohan Pg.No. 525

89. Concise Diagnosis & Manage Henry Pg.No. 198

90. Concise Diagnosis & Manage Henry Pg.No. 198

91. Medicine for Stud. Golwalla Pg. No.14

92. Clinical Pathology by Sarkar Pg.No. 205

93. Medical Technology Pg.No. 198

94. Medical Technology Pg.No. 240

95. Clinical Pathology by Sarkar Pg.No. 199

96. Medical Technology Pg.No. 198

97. Physiology Joshi Pg.No. – 74

98. Physiology Joshi Pg.No. – 74

99. Physiology Joshi Pg.No. – 109

100. Medical Student Biochemistry Pg.No. 201

101. Physiology Joshi Pg.No. – 109

102. Biochemistry for Student Pg.No. 201

103. Physiology Joshi Pg.No. – 109

Drug Review :

104. Thripathi Pharm Pg No. 245

105. B.P.Nighantu Pg.No. 454

106. Pharm. Satoskar Pg.No.71

107. Med. Pharm. Thriphathi Pg.No. 55

108. B.P. 16/17

156  

Discussion :

109. A.Hr.Ni. 12/1 114 Ch.Chi. 28/61

110. Ch.Chi. 15 115. Ch.Chi. 28/223

111. Ch.Vi. 2 116. Ch.Chi. 28/225

112. Ka.Khi. 16/3

113. Ch.Chi. 15

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