Prameha kc015 hyd

A Clinical Study of the Effect of SomarajyadiChurnam In the Management of Prameha.

THESIS SUBMITTED IN PARTIAL FULFILMENTFOR THE DEGREE OF

Doctor Of Medicine (Ayurveda)

ByG.KAVITHA REDDY

B.A.M.S

Under the Guidence of

Dr.V.VIJAYA BABUM.D.(Ay)

Reader/Professor K.CPost Graduate Dept of Kayachikitsa.

Co-GuideDr.Vijaya Lakshmi

M.D (Ay)Gaz.Lecturer Dept.of K.C.

DEPARMENT OF KAYACHIKITSA POST GRADUATE UNITGOVERNMENT AYURVEDIC COLLEGEOsmania University,Hyderabad-A.P.India.

created by technoayurveda.wordpress.com of Dr.KSRPrasad

Ayurmitra

TAyComprehended

CONTENTS

Contents Page Nos.

I Introduction

Historical background of Disease

II Shareeram

III The Disease

1) Nidana

2) Poorvaropa

3) Roopam

4) Classification of Disease

5) Samprapti

6) Upadravas & Aristalakshanas

7) Sadhyaasadhyata & Sapeksha nidana

8) Chikitsa and Pathyaapathya

IV The Drug and its Selection

V Clinical Study

1) Method and Material

2) Observation and Results

VI Discussion

Conclusion

Summary

Bibliography

Case Sheet


Dr.N.T.R.UNIVERSITY OF HEALTH SCIENCESVijayawada

POST GRADUATE TRAINING & RESEARCH UNITDEPARTMENT OF KAYA CHIKITSA

Dr.B.R.K.R.Govt.Ayurvedic College / HospitalHyderabad.

CERTIFICATE

This is to certify that Dr. KAVITHA REDDY, a final year Post Graduate Scholar of

M.D.(Ay) Kaya Chikitsa of this institute has worked for the thesis on the topic “A clinical

study on the effect of Somarajyadi Churnam in the Management of Prameha” for the

degree of Doctor of Medicine (Ayurveda). This work has been completed under my direct

supervision after a series of scientific discussions.

The scholar has put in commendable effort for designing and executing the methods

and plans for the study.

Hence I recommend this dissertation to be submitted for adjudication.

Signature of the Co-guide Signature of the Guide

DR.K.VIJAYA LAXMI DR. V.VIJAYA BABUM.D.(Ayu) M.D.(Ay)Lecturer Reader

Post Graduate Dept. of Kaya ChikitsaDr.B.R.K.R.Govt.Ayurvedic College

Hyderabad


Dr.N.T.R.UNIVERSITY OF HEALTH SCIENCESVijayawada

POST GRADUATE TRAINING & RESEARCH UNITDEPARTMENT OF KAYA CHIKITSA

Dr.B.R.K.R.Govt.Ayurvedic College / HospitalHyderabad.

CERTIFICATE

This is to certify that Dr. KAVITHA REDDY, a final year Post Graduate Scholar of

M.D.(Ay) Kaya Chikitsa of this institute has worked for the thesis on the topic “A clinical

study on the effect of Somarajyadi Churnam in the Management of Prameha” as per

requirements of the order laid by the N.T.R.University of Health Sciences, for the purpose.

The Hypothesis submitted by her in the First year M.D. (Ay) is one and the same to that of

the dissertation submitted.

I am fully satisfied with her work and hereby forward the dissertation for the

evaluation of the adjudicators.

Date:Place: Hyderabad.

Dr. PRAKASH CHANDERM.D.(Ay)

Professor & H.O.DPost Graduate Dept. of Kaya ChikitsaDr.B.R.K.R.Govt. Ayurvedic College

Hyderabad.


A CLINICAL STUDY OF THE EFFECT OFSOMARAJYADI CHURNAM IN THE MANAGEMENT OF PRAMEHA

Dissertation submitted in partial fulfillment for the degree of

DOCTOR OF MEDICINE (AYURVEDA)

In

KAYACHIKITSA

By

Dr. KAVITHA REDDYB.A.M.S

GUIDE

Dr. V.VIJAYA BABUM.D.(Ay)

ReaderPost Graduate Department of Kayachikitsa

Dr. B.R.K.R.Govt.Ayurvedic CollegeHyderabad.

Dr. N.T.R.UNIVERSITY OF HEALTH SCIENCESVIJAYAWADA

Dr.B.R.K.R.Govt. Ayurvedic College, HYDERABAD.

2008


ACKNOWLEDGEMENTS

At the unforgettable moment, I prostrate my head on the feet of our aradhyadeva

LAKSHMI NARASIMHA SWAMY for deputing me to serve the man kind.

I take atmost pleasure and feel privileged to express my deep sense of gratitude and

extreme and Indebtedness to my guru and guide Dr V. VIJAYA BABU M.D(Ayu),

Reader, Post Graduate Dept. of Kayachikitsa, Dr B.R.K.R Govt Ayurvedic

college,Hyderabad. for his constant and valuable guidance, encouragement throughout

the dissertation work and with thought provoking discussions, undoubtedly correct,

affectionate and untiring guidance of my guru has been a greatest asset in completion.

I expresss my heartful gratitude to Dr.PRAKASH CHANDER, M.D(Ayu), Professor and

Head of the Dept, P.G Dept. of Kayachitsta, Dr.B.R.K.R Govt Ayurvedic

college,Hyderabad. For his constant support, guidance, encouragement and kind co

operation in all aspects.

I am highly indebted to Dr. K.VIJAYA LAKSHMI for her valuable suggestions, being a

co-guide.

I take this opportunity to express my sincere thanks to Dr. Nageswer Babu, Dr.M

Ramalingeswar Rao, Dr.Vasudeva Rao, Dr. M.L Naidu, Dr.M.Satya Prasad and technical

assisatants Post Graduate Dept of Kayachikitsa,For their kind co-operation in my clinical

work.

I pay my sincere respect to Dr.M Sadasiva Rao Principal of Dr B.R.K.R Govt Ayurvedic

college,Hyderabad.for providing facilities for the research work.

I am greatful to the Ex -Superintendent Dr L.R. K Murhty Govt Ayurvedic hospital, Dr

B.R.K.R Govt Ayurvedic college,Hyderabad. for their kind co-operation.

I am thankful to Dr.V.L.N Sastry, Superintendent, Ayurvedic

hospital,Erragadda,Hyderabad for permitting me to conduct research work in the hospital.


I am highly thankful to Dr. Ananthasayanachari,HOD of P.G Dept. of SSP and

Dr.M.Philip Anandkumar, HOD of P.G Dept of Dravyaguna for their kindly co-

opearttion.

I cordially Acknowldge my friends and collegues Dr D.Usha Madhuri, Dr.Alibasha,

Dr,Sreenivas Rao, Dr,.Nanda Kumar, Dr.Sivanarayana,Dr.Jaya Lakshmi,Dr.Lavanya, Dr

Padmaja and otheres who helped me in one way or other in completing this work.

I thank to Mr Ramalingeswar Rao for typing this work type neatly.

I thank to Mr Surendra Nath who helped me in statistic analysis.

I express my special to thanks to K.Subba Reddy for contious co-operation and

encoragemnt and concern and care.

I pay homage to my beloved father Mr G.Sidda Reddy and Mrs G.Santhamma.

& my beloved brother Mr. G .Bhanu prakash Reddy their incessant love and blessings

was constant driving force behind my progress.

I am highly greatful to the authors of all the books and articles which have been utilized

by me as the source of information in the preparation of this thesis.

Lastly I am thankful to all my patients of trial drug and all those persons, who have

helped me directly or indirectly for the project work.

Date:

Place: Hyderbad. Dr. Kavitha Reddy


INTRODUCTION

Ayurveda is a science of life. This is most auspicious and scared of all sciences.It is

originated from Atharva Veda.The Rig and Yajurveda also hold substantial role of

Ayurveda. The word Ayurveda has not seen as such in the Vedas but a considerable

portions of the Vedas is devoted for the promotion of long life, prevention of disease and

to medical treatment

Since 19th centuary there has been noted progress in the Indian medicine. Currently

prameha is considered to be due to metabolic disturbance and insulin, Ayurveda has

required an important place in the competitive world along with other branches of

medicine by the special knowledge and modes of treatment of Madhumeha.

Madhumeha is more or less found in all countries. However the incidence is more in the

persons addicted to unwholesome diet and action. A large population of the world

specially persons of Asian subcontinent are afflicted by the disease.

Diabetes was known to ancient Indians as early as 6th centuary2 .Charaka in his Charaka

samhita has mentioned the sweetness of urine in addition to polturia.3 He collected

material from much earlier workers of Agnivesha who based his writing on the teachings

of Atreya who lived in the 6th centuary B.C4.The Indian physician Susrutha in 500 A.D

described the disease as Madhumeha with symptoms of foul breath, voracious appetite

and languor,besides Charaka and Susrutha samhitas. Other early Indian example:Astanga

Hrudaya, Bhavaprakasha, Madhava nidana ,Sarangadhara samhita etc. have also

described Madhumeha as Diabetes.

The Indian indigenous agents can be divided into groups according totheir source of

origin viz. vegetable or herbal and mineral preparations. Vegetable or herbal agents

administered as “swarasa” “kwatha” “churna” “asavas” and “aristas” constitute the

majority of Indian indigenous anti diabeticdrugs. Mineral preparation is given as

“bhasmas” are comparatively fewer. The bulk of information on this indigenous drugs is


scatered in fragments with many individuals and in age old books and manuscripts

which are some time out of print.However a few books examples:- Vaman Ganesh

Desai’s Aushadi sangrah5, Nadkarnis Materia medica6,7 and Chopras indigenous drugs

of India8 and some reviews of Mukerjee9,Ajgonkar10, Chowhan and Sen11 have given

some comprehensive lists of such drugs are claimed to be useful in Diabetes.

A middle aged person, who is apparently normal, may start complaining of weakness,

excessive urination during nights and increase of hunger. Unless these complaints are

voiced by the patients, it is difficult to notice that the person is suffering from disease. On

a through investigation, the person is diagnosed as suffering from Diabetes mellitus

(Madhumeha). Generally Madhumeha is known as a “richmans disease” particularly

because a person who is able to enjoy the pleasure of life (over nutrition) without any

perceptible exercise is usually affected with this disease. The importance of over nutrition

is shown by the fact that over the age of 40, some 80% of the patients developing

diabetes are, have been considerably overweight. The question is relevant that “Every

excess causes a defect, every defect an excess”12. Broadly speaking both the incidence

and mortality of diabetes after middle age vary directly with the degree of obesity.

Madhumeha is achronic disease of relapsing nature13. The disease is also a debilitating

one. The treatment for the disease, at present, in modern science is based on the

additional supply of insulin, which is very disadvantageous to a patient to be continued

indefinetly. Researches are being conducted throughout the world to find permanent cure

for this disease. The efficacy of the Ayurvedic treatment has to be scientifically

investigated thoroughly.

Accordingly care has been taken not only to select a compound drug and simple yoga

from those prescribed for the disease in the sastra, but also to select and easily available

drugs and a yoga which is easy to prepare and administer. The drug selected thus is

“Somarajyadi churnam” and the yoga selected constitute of Bakuchi ,Avarthaki,

Madhunashini, Sunti. It is anubhuta yoga. These drugs collective have got Madhumeha

hara property and also kapha medohara gunas.


Thus ,the aim and scope of the present work has been limited,

1. To a clinical study on prameha/ Madhumeha and,

2. To a clinical study of the effect of Somarajyadi churnam in the management of

prameha.

The disease , the drug and the clinical study are discussed in forth coming pages.

REFERENCES

1. CHARAKA SUTRASTANA 30-21

SUSRUTHA SUTRASTANA 1-8

ANTISEPTIC 57:221 AND 285 1980 BY CHOWHAN &SEN

3.CHARAKA SAMHITA 1940 EDI. P. 675 SRI GULAB KUNVERABA

4.WORLD CONGRESS ON DIABETES IN THE TROPICS, BOMBAY

20TH &22ND JAN.1966 MADHUMEHA 6:289,1966

5.NAGARJUNA, CALCUTTA 4:275 1960

6.INDIAN MATERIAMEDICA VOL.I 548 POPULAR BOOK COMPANY,

BOMBAY, 1954.

7. INDIAN MATERIA MEDICA VOL.I 3RD EDI.239,344 POPULAR BOOK

COMPANY, BOMBAY, 1954

8. CHOPRAS INDIGENOUS DRUGS OF INDIA 2ND ED.P.505,604 ,673 UNDHER

AND SONS PRIVATE LTD.CALCUTTA 1958

9. JOURNAL OF SCIENCE IN INDIAN MEDICINE REVIEW 10 A SUPPLEMENT

1957-1

10. NAGARJUNA, CALCUTTA 4:275,1960

11. NAGARJUNA CALCUTTA 12. ANTISEPTIC57:221,285,1960

12. R.W.EMERSON

13.CHARAKA SUTRASTANA 23/3-4


HISTORY

Study of sequential evolution is primestep in research field. Study of history is

important to know about the systematic development and progress of the subject to

determine the future plans for further establishment and research designing. Here present

review related to prameha is explained.

The evolution of Madhumeha can be traced from Vedas but in rudimentary form,

when we go through the Athrvaveda there is a reference related to the disease ‘Asrava1’

along with its management. Sayanacharya opined that asrava means ‘Mutraatisara’ the

English translator Whitney (1962) interpreted it has Fulx and Griffith (1962) as

morbidflow, while layman has translated the meaning of asrava as Diabetes mellitus2

Sayanacharya highlighted the vatic nature of this ailment.

A)Samhita period :- Explorative discretion of disease Madhumeha occurs at

samhitaperiod .

1)Charaka samhita:- In this ancient treatise of medical science, charaka explained the

etiology, pathogeness, symptomatology, complications and treatment modalites in detail

in Nidana 4th and chikitsa 6th chapter. While in sutra sthana 17th chapter he described the

avaranajanya pathogenesis of Madhumeha, this is the unique contribution of this treatise3

.

2)Susruta samhita:- Susruta also explained Prameha in elaborative manner with separate

chapter on its management. He used ‘Kshoudrameha’ synonym to Madhumeha in nidana

6th chapter. He typically mentioned the kashayas according to each type of prameha and

mentioned the body constitution and symptoms related to sahaja and apathyanimittaja

prameha.

3)Astangahridaya:- Detail description about the disease is given as in charaka and

susrutasamhatas with slight moderations. He added some new herbs and herbal

compounds as well as rasausadhis for the treatment.


4)Harita samhita:- Harita mentioned it as papajanya and enumerated 13 types of

prameha with nomenclature different than above treatise like, puyameha, ghritameha etc.

5)Bhela samhita:- He described prameha is of two types i.e svakrita and prakritameha4 .

6)Kashyapa samhita:- He mentioned the symptoms of prameha child in vedanadhyana

and noted the disease as chirakari.

B) Medievalperiod:- In this period commentaries mainly written, but most of them

contains only the collection of thoughts from previous authors.

1)Madhavanidana:- He collectively repeated the description of charaka, susruta and

vagbhata in 33rd chapter.

2)Gayadasa:- Explained the avilamutrata because of the presence of dooshya in it.

3)Sarangadhara samhita:- Only mentioned the 20 types of prameha in prathama khanda

7th chapter.

4)Bhavaprakasha:- He described prameha and Madhumeha along with some new

herbomineral preparations in madhyama khanda 38th chapter.

5)Yogaratnakara:- Explained prameha and Madhumeha along with treatment.


Historical Milestones

YEAR SCIENTIST INVESTIGATION

1500BC Eberuspapyrus Clinical description of disease.

600BC Charaka Clinical description and noted sweetness

in urine and roll of heredity.

400BC Susruta Just as charaka

BC30-38 Celsus(Greece) Clinical description.

AD30-90 Aretaus(Greece) Name Diabetes was introduced which

means run through.

132-201AD Galen Introduced the term the diarrhoea of the

urine.

860-932AD Rohozes(Percia) Noted sweetness in urine and given

clinical description.

980-1038 Avicenna(Arab) Noted sweetness in urine and given

clinical description.

1135-1204 Smosesmaimomies

(Moraco)

Noted its prevalence in hot countries.

1478-1555 Jaques Dubois

sylvanus(philppines)

Evoparated the specimen of urine of a

diabetic patient and discovered a residue

which was almost glucose.

1511-1568 Arnatusluritanus Outlines dietery regulation for diabetes.

1514-1644 Johanu Baptista Van

Helmant(Belgian)

Given first description of lipomia.

1621-1699 Willis Thomas(Great

Britain)

Started treatment for D.M First.

1637-1698 Mortan Richard(Britain) Roll of heredity in diabetes was

observed.

1653-1727 Brunner J.C(Swiss) Removal of pancreas causes thurst and

polyuria.


1712-1790 Gellura William(Great

Britain)

First to add mellitus to diabetes.

1745-1821 Johanu Peth

Frank(German)

First to Separate Diabetes insipidus

from diabetes mellitus.

1788 Cawles(English) Described pathology of pancreas of

diabetes.

1858-1944 Vonnoorden evienna Belived that liver plays a role in

diabetes.

1869 Langerhan paul(Greek) Discovery of pancreatic islets.

1870 Claude Bernard(France) Noted sugar storage in liver as glucagan

and elevated sugar levels in blood in

diabetic patients.

1874 Kassmaul(German) First described over breathing in

diabetic acidosis.

1889 Von meing &

ninkovaski(German)

Development of diabetes of after

removal of pancreas.

1985 Nonmeyn(German) Hereditary diabetes and its distribution

between juvenile and late onset of

diabetes.

1900 Opic,

Weicuselbalen(American)

Observed islet lesions in D.M

1909 Demeyer Hypothetical view for harmone of is

islets named insulin.

1910-1920 Zulger(German)

Paulaski(Rumania)

Insulin was almost discovered.

1921-1922 Banting and Best(Caneda) Insulin was discovered from dogs and

pancreas.

1923 Hoursay(Argentina) Lessening of pancreatic diabetes by

hypophysectomy.

1936 Longlukens(U.S.A) Lessening of pancreatic diabetes by


adrenalectomi in cats.

1970 onwards Merwin gliedman and

others

Transplant of pancreas, culture of

isletscells of pancreas, transplant of B

cells.

1974-1975 Liebel-Selden(Canada) Artificial pancreas.

References:-

1.Ayurveda Itihas by Dr.P.V.Sharma

2.History of Diabetes from remote to recent times by Dr.K.Raghunathan.

3.Charaka Nidana 8/11

4.Bhelasamhita Nidana 6/1-4


Shareeram

1

SHAREERAM

The word pancreas means pan-all, kreas-fresh. It is a both exocrine & endocrine gland. It lies

transversely across the exterior abdominal wall, behind the stomach, from duodenum to the

spleen at the level of L1 & L2 vetebra. It is J-shaped.

Measurements:-

Length 6-8inches Breadth – 1- ½”

Thickness – ½ - ¾” weight – 90gm

1. Diabets mellitus is a chronic disease due to disordered carbohydrate metabolism and it results

due to deficiency of insulin secreted by the Beta cells of islets of Langerhans of pancreas. But

hormones of pituitary and adrenal glands are also intimately related to the development of

disease state.

2. So the involvement of organs in Diabetes are

1) Pituitary gland 2) Pancreas 3) Adrenal gland 4) Liver

PANCREAS

The pancreas is a compound alveolargland. It has got both exocrine & endocrine

function. During development pancreas lies in the mesoduodenum following the rotation &

ultimate fixation of the gut the pancreas comes to lie against the posterior abdominal wall

behind peritoneum.

The adult pancreas consists of the Head, neck, body & tail. The whole organ is about

15cm long with right margin of the head is in contact with the descending part of the

duodenum & tail in contact with the spleen.

The head of the pancreas which is flattened from before backwards from an

irregularly shaped disc which is thicker than the remainder & lies within the C shaped

duodenal loop at the level of 2nd lumbar vertebrae.

The part of the head which extend to the left behind the superior mesenteric vessel is

known as uncinate Process. The constricted portion or neck connects the head & body of the

pancreas. The neck lies infront of the beginning of portal vein.


Shareeram

2

The body is at first flattened back soon becomes some prismatic in shape with

posteriosuperior and inferior surface and is continued into the tail which is in contact with

spleen.

Anteriorly the body of the pancreas in continued by peritoneum except along the live

of reflexion of mesocolon at the border separating the superior and inferior surfaces.

The superior surface of body and tail is covered by the peritoneum of posterior wall of

the lessersac and is related to the stomach.

The tip of the tail of pancreas is the only part of the whole organ to be completely

surrounded by peritoneum

The pancreas is deeply seated within the abdominal cavity. The normal pancreas is

not palpable.

Ducts of Pancreas

The exocrine secretion of pancreas are discharged into the duodenum through the

pancreatic duct. It commences at the tail of the organ by the union of small ducts in its course

towards the duodenum.

It receives numerous tributaries the ducts from lobules. The duct termination by

giving the bileduct at the hepatopancreatic ampulla.

Microscopic structure:-

The exocrine portion of pancreas consists of acini grouped into lobules. The exocrine

pancreas made up of isolated group of cells the islets of langerhans.

The terminal acini may be tubular in form or rounded.

The acini are lined with pyramidal epithelial cells which rest on a basement

membrane and project toward the lumen of the acinus.

The size of the lumen varies with the functional activities of the acini. During the

secretory pahse granules accumulate in the cells which enlarge and encroach on the lumen.

Several acini join on intercalated duct lined with cuboidal epithelium.

Endocrine portion (Islets of langerhans)

It is an endocrine organ which exert a profound effect on carbohydrate metabolism.


Shareeram

3

The exocrine cells of pancreas are aggregated into small discrete collection of cells of

which there are between one and 2 millions.

Scattered either between acini, between acini & ductules or in interlobular connective

tissue in all parts of pancreas. These cells groups are usually referred as the islets of

langerhans.

The islets are composed of aggregation of epithelial cells associated with capillary

blood vessels. A thin peripheral connective tissue capsule separates the cells from adjacent

exocrine tissue & fine connective tissue extends into the islets along blood vessels.

In endocrine portion 4 cells are present

1) cells

2)cells

3) cells

4) F cells

cells synthesise and secrete glucogon and cells produce insulin and D cells have

been linked with either gastrin or secretin production. F cells secretes pancreatic polypeptide

(PP)

The first harmone to be identified as a product of the islet was insulin. Subsequently

glucagon and gastrin have been identified.

The endocrine pancreas consists of 0.7 – 1 million small endocrine glands – islets of

langerhans – scattered within the glandular substance of the exocrine pancreas.

The islet volume comprises 1-1.5% of the total mass of the pancreas and weighs about

1-2g in adult humans.

F cells which secretes pancreatic polypeptide has been formed primarly in islets in the

posterior portion of the head a discrete lobe of the pancreas separated from the anterior

portion by a facial partition.

The posteriorlobe receives its blood supply from the superior mesenteric artery, the

remainder of the pancreas derives most of its blood flow from the celiac artery.


Shareeram

4

Islets in the posterior lobe area consists of 80-85% F cells 15-20% cells,lessthan

0.5% glucagon producing A cells.

The F cell volume varies with age and sex. The volume tends to be larger in men and

in older persons.

In contrast to the posterior lobe, the pp-poor islets located in the tail, arising from

embryonic dorsalbud, contain predominantly insulin secreting betacells with approximately

20% of the cells being glucagon secreting A cells and about 3-5% D cells that produce

somatostatin.

Islet Vascularisation:

The islets are richly vascularised, receiving 5-10 times the blood flow of a comparable

portion of exocrine pancreatic tissues.

The direction of the blood flow within the islet has been postulated to play a role in

carrying insulin secreted from the antral region of an islet to its peripheralzone – where the

insulin modulates and decreases glucagon release from A cells, which are mainly located on

the periphery of islets.


Shareeram

5

AGNI & ITS IMPORTANCE IN MADHUMEHA

The definition of Kayachikista itself is a treatment to agni but not a disease.

“Kayasya antaragne chikista kayachikista”

Normal state of agni gives health & abnormal state of agni itself is a factor for all Nija

Vyadhis, hence one should protect agni very carefully.

Ayurveda has given much importance to agni in the treatment of diseases, Ahara &

Bhesaja both should be advised based on agnibala of that person.

Aharapachana has been described in Avasthapaka indicating the stages through food

substances in the amasaya & Pakwasaya pass in the course of digestive process.1

(Digestion & Metabolism – Dwarakanath Page.53)

Avasthapaka is divided into two stages. Viz Prapaka has been defined by chakrapani

as Pradhamapaka2 (cha–chi 15/9). The term vipaka meaning is the change to which the food

has undergone. Pradhamaka is again subject to the influence of Jataragni.

Prapaka is mainly related with the food stuff where as vipaka relates to the action of

Jataragni on the drugs. Vipaka is three types: Madhura, Amla, Katu3 (A.H.Su 9/20)

The Prapaka commenses from the time of the food is introduced into Mouth. The

Pranavata main function has the aharagrahana and propels the food in to the Urdwa

amasaya.4 (cha-chi 15/6)

The tridoshas takes place in the digestion of food. If the digestion period is divided

into 3 parts, the first part is having the predominance of Kapha, the second part is

predominance with pitta, and in the third the vata. Therefore the digestion of food or

Aharapachana is divided into 3 stages.5 (A.Hri.Su.1/8)

Madhurabhava Avastha (1st Phase):-

Even though the ingested food contains the 6 Rasas, the first stage of Pachana is

Madhurapaka6 (Su.su–6/1.4) Just after ingestion of the food being digested in the amasaya

attains first the MadhuraRasa and then leads to the formation of Kapha, which is phenila in


Shareeram

6

appearance7 and the food that is propelled into amasaya mixes with drava.which is present

in this organ is doing bhinnasanghatam. 8(i.e the food is broken down and softened)

Role of Kledakakapha:-

Kledaka kapha is stated to be located in Amasaya. Its function is to moisterise food brought

to this site, disintegrates, breaks & liquefies9 (chakrapani on cha.su 20/8). Kledakakapha

protects the amasaya from being digested by the pitta which is also located there10

(A.H.Su.12/16).). It should be noted that the rasa of kapha is Madhura.11 (Su.su. 21/16).

Amlabhava avastha (2nd Stage):-

The partly digested food entering into adhoamasaya from urdwamasaya, enters into

the amlapaka with predominance of pitta. There will be abundant production of Achyapitta

in its immature stage is amla. 12(Cha.chi 15/9). The outcome of this phase of digestion is

the production of acidified change i.e. Pakwapakwa or kinchit Pakwa. 13(Digeston &

Metabolism in Ayu. C.Dwaraka nath)

The food in this stage is not yet fit for absorption & utilisation in metabolism

14(Chakrapani on cha.chi 15/10)

In this stage of digestion there will be two important events.

1. The Rasa of the end product of this stage is amla.

2. The end product of this stage is achyapitta.

Samanavata & Pachakapitta play an important role in this process.

Samanavata:-

The function of Samanavata quoted by Charaka as stimulation to agni to digestion of

food 15. After digestion is completed, helps in separation of Sara & Kitta. Sarangadhara

quoted the meaning of Samyak, as it will spread equally to all directions 16. (Sa.poo. 5th

Chapter)

According to Vagbhata, the Samanavata received the food into the annavahasrotas

(grihnati), Retains it till the digestion is completed (pachati), separates the sara from kitta


Shareeram

7

(vivechayati) & finally propels the kitta to the later parts of the annavaha srotas

17(A.Hri.Su.12/8) (Munchati).

Pachakapitta:-

The Pachakapitta which digests the food is stated to be the Controller of remains

pittas. Their functions are depended upon the increase and decrease of Pachaka pitta 18

(cha.chi.15/39)

Susruta & Vagbhata quoted its location in the interior of amasaya and Pakwasaya.19

(Su.Su.21/10) Charaka mentioned these two asayas as kosta and here digestion takes place.

Both these asayas have in inner layer called Pittadharakala20. (A.Hrisa.3/50)Which

produces Pachakapitta which digests the ahara & separates it into Sarabhaga, Mutrabhaga &

Pureeshabhaga.

Pittadharakala:-

Located in the amasaya & Pakwasaya this part of annavahasrotas retains the food

upto its completely digestion, it is called Grahani. The function of this kala is to support the

Pachakapitta which is helpful for digestion of food. It aids in seperation of the Sara &

Kitta21. (Digestion & Metabolism –Dwarakanath)

Katuavastha (3rd Stage):-

The partial digested food then propelled from the adhoamasaya into the Pakwasaya

to complete its digestion. The digested food separated into Sara and Kitta. The annarasa is

absorbed from the Kudyas of Pakwasaya & Circulated through out the body by the

dhamanies 22 (cha.chi.15/36)

The fluid part of the Kitta is also absorbed, thereby rending it into a dry and light

mass, and pureesha in the Pakwasaya during this process is produced the vata which is katu

in nature 23 (cha.chi.15/11) .The Sahajakrimis which reside here will help in the production

of vata.

The fluid part of the kitta is absorbed by the kudyas of Pakwasaya, constitute the

mootra and is excreted through vasti. The Rasa of the pitta is katu. According to the third


Shareeram

8

stage the digestion of the food is stated as Katuavastha 24. (Su.Ni.3/21-22)Its clear that the

end products of this stage is katurasa, and vata which is pungent in nature.

* * * * *


Shareeram

9

INSULIN AND ITS ROLE IN DM

Insulin Synthesis :- Robbins Pathology

Gyton Physiology

S.No. Site Activity

1. Rough

E.R

Translation of m–RNA on beta cell of Pancreas itself where

Humaninsulin gene is expressed.

2.

3.

E.R

Glogi

apparatus

Preproinsulin – mol. wt. 11,500

Proteolytic Clearage of Prepeptide

Proinsulin

Cleavage of c–peptede

Insulin C–Peptide

Insulin and C–peptide will be secreted simultaneously after physiological stimulation.

Chemistry of Insulin:- (Pharmacology & Pharmacotherapeutics)

Insulin is a harmone secreted by the beta cells of this islets of Langerhans of

Pancreas & derives its name from the Laitn word ‘Insula’ which means an island. It was

extracted from the pancreas by Banting & Best in 1921 & was isolated in crystalline form

by Abel in 1930.

Insulin is a polypeptide with a molecular weight of about 6000, consisting of two

amino acid chains, A&B, linked by two disulphide bridges.

The Chains Contain 21 & 30 amino acids respectively, all in a known sequence. The

disulphide bridges are essential for its biological activity.


Shareeram

10

Insulin is soluble in water but undergoes molecular aggregation at extremities of PH

(3.2 & 10) such aggregation is further enhanced by the presence of zinc which brings about

crystallisation of insulin.

Transport, fate & excretion: -

In the blood insulin circulates in unbound form. The average plasma half life of

insulin is 6 minutes. So that it is mainly cleared from the circulation with in 10–15min.

except for that portion of insulin which is combined with the receptors of the target cells.

The remaining is mainly degraded by the enzyme insulinase in the liver and to a lesser

extent in the Kidneys.

Only traces of free insulin appear in the Urine. Insulin degradation is retarded in

chronic renal disease.

Factors influencing the insulin release:-

Stimulators Inhibitors

1. Glucose 1. Somatostatin

2. Mannose 2. 2 – Deoxy Glucose

3.Amino acids (Leucin), arginnine etc) 3. Mannoheptulose

4. Intestinal Harmones

(GIP, Gastrin, Secretin, CCK,

Glucagan & others)

4.

– adrenergec stimulating

agents (Norepinephrine,

epinephrine)

5.– Keto acids 5.

– adrenergic stimulating

agents (Propranolol)

6. Acetylcholines 6. Diazoxide

7. Glucagon 7. Thiazide diuretics

8. Cyclic AMP and various cyclic AMP

generating substances8. K+ depletion

9. B adrenergic stimulating agents 9. Phenytoin

10. Theophylline 10. Alloxan

11. Sulphonylureas 11. Microtubule inhibitors


Shareeram

11

Tissues in which insulin facilitates Glucose uptake:-

1. Skeletal Muscle 6. Crystalline lens of the eye

2. Cardiac Muscle 7. Pituitary Gland

3. Smooth Muscle 8. Fibroblast

4. Adipose tissue 9. Mammary glands

5. Leucocytes 10. Aorta

11.Alfa Cells of Pancreatic Islets

Tissues in which Insulin does not facilitates Glucose uptake:-

1. Brain except part of Hypothalamus.

2. Kidney tubules.

3. Intestinal Mucosa

4. R.B.C

Mechanism of Insulin Secretion:-

Increased Sugar level

Translation GLUT(Insulin dependent Glucose Transporting protein)

Uptake of Glucose by cells

Release of Insulin

If Stimulation Persist

Active synthesis of Insulin


Shareeram

12

D) On Iron Transport:

It favours movement of K+ into cells.

E) On Growth & development.

F) Nucleus:

Stimulation of DNA Synthesis, cell Proliferation & differentiation.

G) Vascular endothelium:-

Stimulates lipoprotein lipase on the surface of the vascular endothelium.

Principal action of Insulin on Various tissues:-

A) Adipose Tissue:-

Increases Glucose entry

Increases Fatty acid synthesis

Increases Glycerol Phosphate synthesis

Increases triglyceride deposition

Activation of Lipoprotein lipase.

Inhibition of harmone sensitive lipase

Increases K+ uptake.

B) Muscle Tissue:-

Increases Glucose entry.

Increases Glycogen synthesis

Increases amino acid uptake

Increases Protein synthesis in ribosomes.

Increases Protein Metabolism.

Increases release of gluconeogenic amino acids.


Shareeram

13

Increases Ketone uptake.

Increases K+ uptake.

C) Liver:-

Decreases ATP

Decreases Ketogenesis

Increases Protein synthesis

Increases lipid synthesis

Decreases glucose output by decreasing gluconeogenesis and increasing glycogen

synthesis.

Biological Effects of Insulin:-

A) On Carbohydrate Metabolism:-

1. Reduces the rate of release of glucose from liver.

By inhibiting glycogenolysis

By stimulating glycogen synthesis

By stimulating Glycolysis

By indirectly inhibiting gluconeogenesis via inhibition of fatty acid

mobilisation from adipose tissue.

2) Increases rate of glucose uptake into all insulin sensitive tissues notably muscles and

adipose tissue.

Directly by stimulating glucose transport across the Plasma

Membrane.

Indirectly by reducing Plasma free fatty acid levels.

B) On Lipid Metabolism:-

1. Reduces the rate of release of free fatty acids from adipose tissue.


Shareeram

14

2. Stimulates fatty acids synthesis and also conversion of fatty acids to triglycerides

in liver.

C) On Protein Metabolism:-

1. Stimulates transport of free amino acids across the plasma Membrane in liver

and muscle.

2. Stimulates protein bio synthesis and reduces release of amino acid from muscle

References:-

1.Digestion&metabolism- c.Dwarakanath page.53

2. CHA.CHI 15/9

3.A.H.SU 9/20

4.CHA.CHI 15/6

5.A.H.SU 1/8

6.SAR.POO 6/1-4

7.CHA.CHI 15/9

8.CHA.CHI 15/6

SU.SU 21/16

9.SU.SU 21/15

10.CHAKRAPANI ON CHA.SU 20/8

11.A.H.SU 12/16

12.CHA.CHI 15/9

13.DIGESTION&METABOLISM-DWARAKANATH

14.CHAKRHI 15/39

15.SU.SU 21/10APANI ON CHA.CHI 15/10

16.CHA.CHI 28/8


Shareeram

15

17.SAR.POO 5 CHAP

18.A.H.SU 12/8

19.CHA.CHI 15/39

20. SU.SU 21/10

21.A.H.SA 3/50

22.DIGESTION&METABOLISM-BWARAKANATH

23.CHA.CHI 15/16

24.CHA.CHI 15/11

25.SU.NI 3/21-22


Nidana

1

NIDANA

Nidana of prameha includes nidana factor mentioned for all 3 doshas as pathogenesis

of Madhumeha involves three doshas. Individual Nidana for premeha of each dosha were

mentioned in Charaka Nidana 4th Chapter.

Various etiological factors mentioned by Ayurvedic Acharyas.

S.No Nidana Reference

1. Asyasukham Ch

2. Swapnasukham Ch

3. Dadhi Ch, B.P

4. Gramya, anupa, oudaka – Mamsa Rasa Sevana Cha, A.H., A.S.

5. Ksheeram Charaka

6. Navannapanam, Navadravyas, Navadhanya Ch, A.S., A.H. B.P.

7. Gudavikaras & Guda Ch, A.S., A.H., B.P

8. All the Ahara Vihara factors which vitiate

medas, Kapha, mutra

Su, A.S., A.H.

9. Madhura rasa, Amlarasa, Lavanarasa – Ahara

having these Rassas

Su, A.H., A.S.

10 Annapana having Snigdna, guru, picchila, Seeta,

drava, Medokara gunas

Ch, A.H., A.S., Su

11. Sura A.S., A.H.

12. Navamadhyam Ch., B.R

13. Gorasam Ch, A.H., A.S.

14. Ekasthanasanarati, Sayyasanaswapna Sukham Ch, A.S., A.H.

15. Diwaswapnam Ch. Su.


Nidana

2

16. Avyayamam Su.

17. Alasyam Su.

18. Recipes prepared with Guda & Pista Cha.

19. Chestadwesta Ch. Nidana

20. Mandostahata Ch. Nidana

21. Atisthulata Ch. Nidana

22. Atisnigdhata Ch. Nidana

23. Mahasanam Ch. Nidana

24. Beejadosha Ch.Chi. Stnana

25. Improper treatment of other Premehas Su

26. Dhumapanam B.R.

27. Ikshu A.S, A.H.

28. Sayanam Vidhivarjitam A.S, A.H.

29. Dustamedas Ch, Su

30. Abaddamedas & Mamsa Ch.Chi

31. Snanadwesham Ch. Nidana

32. Chankramana dwesham Ch. Nidana

33. Intercourse with animals like horse, elephant etc,

mother, sister and intercourse in festival and odd

days.

Vaidhya chintamani

Ayurvedic Acharyars mentioned Hereditary origin of Madhumeha which involves

genes, in those ancient days itself. It was mentioned as beejadosha and Madhumeha

was mentioned as Kulajavikara.


Nidana

3

Dalhana mentioned that females are less prone to premeha or Madhumeha does not

occur in females as Rutasrava in every eliminates all the impurities & purifies all

dhatus. Author of yogaratnakara followed susruta’s version.

Samanya Nidana:-

The keyword in Samanyanidana of prameha is the hetu, which causes Kaphavridii

(kaphakriccha sarvam)8 Kapha is the maindosha involved in prameha and hence all those

hetu that cause Kaphavriddi automatically becomes the hetu for prameha9.

The Samanyanidana can again be classified as

a) Ahara Sambandha b) Vihara Sambandha

a) Ahara10:- Any ahara which is Madhura & lavanarasa pradhana, guru, Manda, Sheeta,

Snighdha, Slakshna, Sandra Stira, Madhuravipaka and Sheetaveerya, these effects

mainly effects the medas and Kleda leading to madhumeha due to Avarana.

b) Vihara11, 12:-

1) Atinidra: Aggravates Kapha and tamasa guna resulting in accumulation of medas

2) Asyasukha: Leading to Kaphavriddi.

3) Avyayam: Results in accumulation of medas & Kapha.

4) Alasyam: results in inactivity causing excessive nourishment. This mainly because

of Kapha and meda.

5) Samasodhana varjana: Causes medas and Kaphakshaya, accumulation of kapha and

medas.

Visesha Nidana:-

1) Kaphaja prameha Nidana: Are the same as explained in samanyanidana because

kapha is dosha visesha in prameha but it should be in bahudrava.

2) Pittaja prameha Nidana13:

Ahara:- ushanagunaahara atisevana, Arularasa, Lavanarasa, katurasa ahara atisevana,

vishamaaharasevana

Vihara:- Ati atapasevana, Atisantapa, Shrama, Krodha

3) Vatajaprameha nidana: The causes for aggravation of vata can be mainly grouped

into two categories

1) Margavarana14 2) Dhatukshaya15.


Nidana

4

The margavarana is a result of accumulation of kapha or pittadosha in the

vatavahasrotas due to respective Nidanasevana, this leads to vataja prameha.

In prameha, dhatukshaya is an invariable consequence of aparipakvata of dhatu. This

leads to aggravation of vata causing vatajaprameha.

Sahaja (Hereditary):- Susrutha mentioned the sahaja word showing genetic predisposition

in the pathophysiology of the disease Madhumeha16. charaka while describing the

prognosis of Madhumeha clearly noted that this is kulajavikara resulting due to defect

in the beeja.

Chakrapani opines that it can cause by Father, Mother or Grandparents, it means the

disease inherited from generation to generation.

Charaka narrated that sahaja type of diseases can occur due to defect in beeja,

beejabhaga or beejabhaga avayava. We can correlate beeja to ovum and sperm,

beejabaga to chromosomes & beejabhaga avayava to genetic coding. Charaka

narrated that indulgence of madhurarasa by mother at time of pregnancy causes

madhumeha & stoulya17.


Nidana

5

NIDANA AND GUNA KARMA

Nidana Predominant of Rasa, Guna

Veerya, vipaka

Vitiates

1) Gurugunaahara Prithvi AP Madhurarasa Kapha, Medas

2) Srigdhagunaahara Pritvi, AP Kleda

3) Dravagunaahara AP Kapha & Kleda

4) Pichilagunaahara Prithvi, AP Kapha & Kleda

5) Seetagunaahara with

dravaguna

AP Udaka & Vata

6) Madhurarasa ahara Snigdha, Guru

Sheetaveerya

Madhuravipaka

Kapha, Rasa,

Rakta mamsa,

Medas. Majja,

Sakra, ojus

7) Lavanarasa ahara Kleda,

Kaphavilayana

Milk and Its Products

8) Goksheera Kapha& medas

9) Mahisha Ksheera Atisneha, Atinidra

Mandagni

Abhishyandi

Kapha&Medas

10) Avika ksheera Pitta and kapha

11) Dadhi Kapha&Medas

12) Godadhi Kapha&Medas

13) Mahisha dadhi Kapha&Medas

14) Avika dadhi More abhishyandi Kapha&Medas

15) Mandaka Mootrala Tridosha


Nidana

6

Ghrita

16) Goghrita Kapha&Medas

17) Mahisha ghrita Kapha& medas

18) Piyusha, Kilata Sugarcane & its

products

Kapha

19) Ikshu Madhurarasa

sheetaveerya

snigdha&Saraguna

Kapha

20) Phanita Guruguna Guru in guna

abhishyundhi

kshara, madhura in

rasa, Snighdha

sheeta in guna &

veerya

Tridosha

Kapha&Medas

21) Matsyandika,

Khandasarkara

Snigdha, guru

madhurarasa

Kapha&Medas

Vegetables (Shaka)

1) Trapusha (Cucumis sativa) Guruguna Kapha, Medas

2) Kadamba Sheetaveerya,

madhura rasa

Kapha, Medas & Mootra

3) Shrungataka

4) Shaluka

5) Kasheruka

Guruguna,

Seetaveerya &

vishtambhi in natureKapha & medas

6) Kumudha Sheetaveerya Kapha & Vayu


Nidana

7

7) Utphala, nala, phala &

Puspa

Madhura, Kashaya in

rasa

8) Vidarikanda Madhurarasa,

Sheetaveerya Balya,

Mootrala in action

Mootra & Kapha

9) Upodika

(Basellacordifolia)

Madhurarasa& vipaka,

Snigdha Sheetaveerya

Kapha

Vihara

1) Nidraatisukha Increases tamoguna Sleshma vardhana

2) Asyaatisukha Increases tamoguna Sleshma vardhana

3) Diwaswapna Increases tamoguna Sleshma vardhana

4) Mrujavarjana Inactiveness, Laziness Kapha & Medas

5) Tyaktavyayama Increases agnimadhya

shareera gourava

Kapha & medas

6) Alasyaprasakta Kapha

7) Failure to perform

samsodhana therapy

Tridosha


Nidana

8

AETIOLOGY

Genetics18,19,20:- The mechanism of inheritance of DM either insulindependant or

noninsulindependent is unclear.

Genetic Susceptibility of IDDM:- This probably involves more than onegene. Candidate

loci have been proposed on chromosomes 2, 6, 11 & 15 though primary geneticsite in

humans is believed to be located in the major histocompatability locous on the

shortarm of the 6th chromosome.

While definite associations exists between class I alleles & type I DM, the D locus is

considered of primary importance encoded by the major histocompatibility complex

(MHC) found to be closely associated with IDDM

Genetic Susceptibity in NIDDM:- Modes of inheritance of NIDDM in variant called

matarityomet DM of the young (MODY) have been more or less conclusive than the

other forms

The concordance rate for DM in monozygotictwins with type 2 disease may be as

high as 80% risk of offspring and siblings of patients with NIDDM are higher than in

type I DM.

Autoimmurity:- The autoimmune destruction of the B cells may be best explained by the

existence of B cell specific protein that for unknown reasons acquires autoantigenic

properties and eventually becomes target for autotimmune reaction.

Heredity:- The mechanism of inheritance of IDDM is unclear. The chance of a child

developing type-1 DM when another first degree relative has the disease is only 5-

10%. HLA identity in a sibling increases the risk.

The presence of NIDDM in a parent increases the risk for IDDM in the offspring

The risk of type I DM is upto 5 times higher when the father has the disease than

when the mother is a diabetic

Environmental Factors:

Viralinfection:- Preceding episodes of infections of Mumps, hepatitis, infectious

mononucleosis and coxsackie virus. Support for viral theory comes from the

observation, that about 1/5th of individuals with congenital rubella develop DM.

Bovine albumin:- It has been suggested that exposure to cow’s milk or milk products early

in life predisposes to autoimmune DM


Nidana

9

Obesity:- Type 2 DM is almost nonexistent in individuals with a body manindex (BMI)

below 22kg/m2 and increased risk of DM with obesity has a strong familial tendency.

Lifestyle:- Epidemiological studies of type 2DM provide evidence that overeating, especially

when combined with obesity & underactivity associated with type 2 DM.

Malnutrition:- It is proposed that malnutrition in utero and in infancy may damage Beta cell

development and causes type 2 DM at a laterstage.

Chemicals:- Alloxan, Glyoxal streptozotocin, Asparyinone, Pentamidine esthionate.

References:-

1.CHA.CHI 6/4

2.CHA.NI 4/4

3.A.H.NI 10/1-3

4.A.S.NI 10/3

5. SU.NI 6/3

6.CHA.NI 4/50-52

7.CHA.SU 23/3-7

8.CHA.NI 4/25

9.CHA.NI 4/34

10.CHA.SU 17/77,78,79

11.CHA.NI 4/36

12.CHA.NI 4/34

13.CHA.CHI 6/2

14.CHA.NI 4/47

15.CHA.NI 6/3

16.CHA.CHI 6/55

17.CHA.NI 6/3

18.Davidson’s principles of Medicine edition 1995

19.Harrison’s principles of Internal Medicine vol 1&2

20.Anderson’s pathology 10th edition,1996


Poorva Rupa

1

POORVA RUPA

PoorvaRupa (Premonitory Symptoms) mentioned by various (1, 2, 3)

S.No Poorva Rupa Reference

1. Jatileebhavam Kesheshu Ch.Ni, Su.Ni, A.S.Ni

2. Asyamadhuryam Ch.Ni, Ch.Chi, A.S.ni, A.H., Ni

3. Karapada suptata Ch. Ni

4. Karapadadaha Chi.Ni, Cha.chi, Su.Ni, A.H.Ni

5. Mukhatalukanta sosha, talugala sosha Ch.Ni, Ch.Chi. Su.Ni, A.S.Ni

6. Pipasa Su.Ni, A.S.Ni. A.H.Ni

7. Thrut Chi. Ni

8. Kayemalam Ch.Ni, A.S.Ni

9. Kayachidreshupadeham Ch.Ni

10. Paridaham Ch.Ni. A.S.Ni

11. Angeshusuptata Ch.Ni., A.S.Ni

12. Mutrebhidravanti pipeelikanam

Mutrechnamutradosham

Ch.Ni.ch.Chi, A.S.Ni

13. Shatpadapipeelikabiccha shareera

Mutrabhisaranam

Ch. Ni

14. Shareeravisragandhata Ch.Ni

15. Nidra Ch.Ni, A.S.Ni

16. Tandra Ch.Ni. Su.Ni, A.S.Ni.

17. Swedam Ch.Chi, A.H.Ni

18. Angagandhata Ch.Chi, A.H.Ni

19. Shitilanghata Ch.Chi, A.H.Ni


Poorva Rupa

2

20. Sayyasanaswapnasukhe Rati Ch.chi, A.h.Ni

21. Hrunnetrajihwasya Sravanopadeha Ch.Chi, A.h.Ni

22. Ghanangata Ch.Chi, A.H.Ni

23. Keshanakhavriddi Su.Ni,. A.H.Ni

24. Seetapriyatwam Ch.Chi, Su.Ni, A.H.Ni

25. Snigdha picchila gurugathram Su.Ni

26. Madhurasukla mutrata Su.Ni, A.S.Ni

27. Saada

28. Durgandhata Su.Ni

29. Swasa Su.Ni, A.S.Ni

30. Talugalajihwa, Danteshu Malotpatti Su.Ni

31. Snigdhangata A.S.Ni

32. Alasyam A.S.Ni

Prameha/Madhumeha involves dravarupa & abaddamedas and Mamsa which causes

premonitory symptoms like

1) Sweda

2) Snigdhapicchilagurugatrata

3) Ghanangata

4) Durgandata

5) Visragandhata

6) Visragandanata

7) Alasyam

8) Sayyasanaswapnasukha Rati

9) Swasa

10) Snigdhangata

11) Trut


Poorva Rupa

3

12) Pipasa

13) Sithilangata

Arambhaka dosha is kapha, aggrevation causes premonitory symptoms like

1) Asyamadhuryam

2) Nidra

3) tandra

4) Madhurasukla mutrata as mutra is a seat of kapha

5) Hrunnetra jihwasya sravanopadeham

According to the involvement of dosha and dooshya combinations all premonitory

symptoms or half of the premonitory symptoms will develop.

References:-

1. CHA.NIi 4/41

CHA.CHI 6/12,13

SU.NI 6/5

A.H.NI 10-38/39

CHA.NI 4/47

2. Godbole,Aravinda. DM for practitioners 1st edition 1974.


Poorva Rupa

4

Pre-diabetic States2

Sometimes a patient with abnormal hyperglycemia may not have full clinical symptoms of

diabetes mellitus and often pre-diabetic states are asymptomatic. Mildsymptoms if

manifested go unrecognized but the identification of such stages can go a longway in

prevention of an overt disease.

The British diabetic association has suggested a classification that is accepted by

WHO expert committee on diabetes. They are as follows:

Potential DiabetesThese are persons who have high probability of developing diabetes. They do not

show any evidence of impaired glucose tolerance. They include.

1) Identical twin of diabetic

2) Persons with both the parents are diabetic

3) Persons with one parent diabetic, the other non-diabetic parent having a diabetic

parent or a diabetic sibling.

Latent Diabetes:a) Persons with normal G.T.T. at present but had an abnormal G.T.T. sometime in the

past viz, during pregnancy, infection when under stress or when obese.

b) Persons with a normal G.T.T. understand conditions but an abnormal one with

provocative tests.

Asymptomatic Diabetes:This stage is variously known as clinical, sub clinical diabetes. They always show an

abnormal G.T.T. but the fasting blood levels may be normal in the early stage. Later on, even

these levels may be raised.


Roopa

1

ROOPA

Roopa of a disease will be produced in the fifth stage of samprapti i.e., Vyaktavasta. Laxana

of Madhumeha mainly grouped under two categories i.e.,

A) Samanyalakshanas:

1) Prabhootamootrata: This is the cordinal sign described by all acharyas. Vagbhata

mentioned prameha as the disease of mutratipravritaja vikara. Patient voids urine more in

quantity and frequency1 . Gayadas opines that this excess urine quantity is because of

liquification of the dushyas and their amalgamation2.

2) Avilamootrata: Patient voids urine having turbidity.

B) Vishistalaxanas3:

1) Madhurata – This is entirely due to Apakva ojus.

2) Rooksha – Rookshaguna is due to vata

3) Pandu – The urine would have lost its normal varna as a result of abnormally

increased shareerakleda.

4) Kashaya – It is a terminal manifestation of DM.

5) Madhusamamootra – Varna, Gandha, Rassa of mootra will be similar to that of

Madhu. It is due to ojonisraana in mootra.

Sarvadaihika Laxana4.

Sahaja Apathyanimihaja

1) Krisha(Emaciated) 1) Stulatwa (obese)

2) Ruksha (dryness of body) 2) Snigdha (Unctous)

3) Alpasi (poor eatingdesire) 3) Bahwasi (polyphagia)

4) Pipasabhrusam(intense thirst) 4) Shayya Asana Sukham (desirous for

posture and lying down on bed)

5) Parisaranasheela (Tendency of roming) 5) Swapnashila (constant tendency for

sleeping)


Roopa

2

Pratyatmaroopa5, 6, 7

Kaphajaprameha

Prameha Mootralaxana

1) Udakameha Accha, Bahusita, Sheeta, Nirgandha udakopama

2) Ikshuvalika Atyantamadhura, Seeta, ishatpicchilam Avilam,

Kandekshurasa Sankasham

3) Sandrameha Paryushita, Sandribhavati bhajane

4) Sandraprasadameha Samhayante mootram

5) Shuklameha Shukla, Pishtanibham, Abhikshnam

6) Sukrameha Athyantamadhuram, Seetam

7) Sheetameha Athyantamadhuram, Seetam

8) Sikatameha Katinamootrata

9) Sanairmeha Mandam, Mandavegam, Kruchram

10) Alalameha Tantubaddaiva, Alalam, Picchilam

11) Surameha Suratulyam

12) Lavanameha(su.ni6/8) Vishada, Lavanatulyam

13) Pishtameha(su.ni68) Pishtarasa Tulyam

14) Phenameha(su.ni6/8) Stokam Stokam, Saphena

Pittajaprameha

1) Ksharameha Ksharatulyavarna, rasa, Sparsha

2) Kalameha Masivarna, Ajasram, Ushnamootra

3) Neelameha Chashapakshinibham, Amlam

4) Raktameha Visra, Lavanam, ushnam, Raktam

5) Manjistameha Visra Lavanam, Ushnam, Raktam


Roopa

3

6) Haridrameha Haridrodakasankasha, Katuka

7) Amlameha(su.ni6/8) Amlarasa, Amlagandha

Vataja Prameha

1) Vasameha Vasamishram, vasabham

2) Majjameha Majjabham

3) Hastimeha Hastimattaiva ajasram, Lasika

4) Madhumeha / Kshoudra meha(su.ni6/8) Kashaya, Madhura, panduvarnata, Ruksha

5) Sarpirmeha Sarpiprakasham


Roopa

4

Clinical Features8

The manifestation of symptomatic Diabetes mellitus vary from patient to patient.

Most often, Symptoms are due to hyperglycemia (polyuria, polydipsia, polyphagia)

but the first event may be on acute metabolic decompensation resulting in diabetic

coma.

Typically, the clinical features of IDDM and NIDDM are distinctive

Insulin Dependent Diabetes:

IDDM usually begins before age 40. Some patients develop type 1 diabetes late in life

with a fist episode of ketoacidosis occurring at age of 50 or even later in rare

instances.

Onset of symptoms may be abrupt, with thirst, excessive urination, increased appetite

and weightloss developing over several days.

In some cases, the disease is heralded by the appearance of ketoacidosis during an

intercurrent illness or following surgery

As outlined in type 1 patient may have normal weight or may be wasted, depending

on the length of time between onset of symptoms and start of treatment

characteristically, the plasma insulinlevel is low or immeasurable.

Once symptoms develop, insulin therapy is required.

Noninsulin Dependent Diabetes:

NIDDM usually begins in middle life or later. The typical patient is overweight.

Symptoms begin gradually and the diagnosis is made frequently when an

asymptomatic person is found to have an elevated plasmaglucoselevel.

In contrast to IDDM, plasma insulinlevels are normal to high in absoluteterms,

although they are lower than predicted for the level of the plasma glucose stated in

another way, if plasma glucose concentrations in nondiabetic subjects were raised to

levels equivalent to those found in NIDDM patients, insulin values would be higher in

the normal group. This relative deficiency reflects the previously mentioned insulin

secretory defect in NIDDM.

For unknown reasons, patients with NIDDM do not develop ketoacidosis but are

susceptible to development of hyperosmolar, nonketotic coma.


Roopa

5

Symptoms:

1) Excessive appetite and polyphagia8

Excessive hunger is due to inability of the tissue to use glucose and loss of fuel in the

urine.

2) Loss of Weight:

Loss of weight in the diabetic may be attributed to the mobilization of fat stores and

breakdown of protein. In addition there may be considerable calorie loss in the urine.

3) Fatigue – Fatigue is due to inefficient utilization of glucose or electrolyte losses prone

to muscular weakness which is the basis of fatigue.

4) Thirst and polyuria – due to loss of water from osmotic diuresis

5) Pruritis Valvae: it is a symptom in 2/3 or all women who develop diabetes

Glucose favours the development of the mycosis and that glycosuria is the underlying

cause.

6) Balanitis

7) Myopia

8) Drymouth

9) Nocturia

10) Wasting

11) Abnormalities of taste

12) White marks on clothing

13) Impotence

14) Amenorrhoea

15) Infection – especially in the skin or failure of wounds to heal


Roopa

6

References:

1) A.NI – 10/7

2) SU.CHI 11/2

3) SU.CHI 11/3

4) SU.CHI 11/14

5) CHA.NI 4/41

6) SU.NI 6/8

7) A.H.Ni 10/35-34


Classification

1

CLASSIFICATION

Though all the three doshas are involved in the pathogenesis of prameha, it is according to

the predominance of dosha the classification was made. The physical characters like varna,

Rasa, Sparsa, of each type of prameha are according to the dosha, dooshya, mala, ahara &

their combination.

Classification of Prameha

I 1) Kaphaja - 10 types - sadhya

2) Pitttaja - 6 types - Yapya

3) Vataja - 4 types - Asadhya (A/c to Charaka)

II 1) Sahaja - Due to beejadosha

2) Apathyanimittaja Due to irregular & faulty diethabits (A/c Susruta)

III A/c to the line of treatment

1) Stula 2) Krisha

IV 1) Sadhya 2) Yapya 3) Asadhya

V Author Yogaratnakara has given the treatment of Dwandajaprameha in prameha

chapter.

Classification of Prameha

Dosha Charaka Susruta Vagwnata

Kaphaja 10 types 1) udakameha

2) Ikshumeha

3) Sikatameha

4) Sanairmeha

5) Sandrameha

6) Sukrameha

7) Shukla meha

8) Sandraprasada

Udakameha

Ikshumeha

Sikatameha

Sanairmeha

Sandrameha

Sukrameha

Pistameha(su.ni6/8)

Surameha(su.ni6/8)

Udakameha

Ikshumeha

Sikatameha

Sanairmeha

Sandrameha

Sukrameha

Pistameha

Seetameha


Classification

2

9) Seetameha

10) Alalameha

Lavanameha

Phenameha

Alalameha

Pittaja 6 types 1) Ksharameha

2) Kalameha

3) Neelameha

4) Lohitameha(ch.ni

4/24)

5) Manjistameha

6) Haridrameha

Ksharameha

Neelameha

Sonitameha

Manjistameha

Haridrameha

Amlameha(su.ni6/8)

Ksharameha

Kalameha

Neelameha

Raktameha

Manjistameha

Haridrameha

Vataja 4 types 1) Vasameha

2) Majjameha

3) Hastimeha

4) Madhumeha

Vasameha

Hastimeha

Kshoudrameha(su.ni6/8)

Sarpirmeha

Vasameha

Majjameha

Hastimeha

Madhumeha

Sandraprasadameha of charaka & Surameha of vagbhata & susruta can be considered

as it.

Lohitameha of charaka, Sonitameta & Raktameha of susruta & vagbhata can be

considered as it.

Majjameha of charaka & Sarpirmeha of susrata can be considered as it.

Classification of Madhumeha

I 1) Dosha Avrutajanya2.

2) Dhatukshayajanya

Vagbhata & Y.R. mentioned this classification (A.H.N 10/21)

1) Doshavrutajanya: This type of Madhumeha is due to Avruta of Vatamarga by the

doshas. In this symptoms manifests according to the Avrutadosha. This type is

kashtasadhya.

2) Dhatukshayajanya: In this type of Madhumeha dhatukshya is due to


Classification

3

i) Rukshaguna of vayu

ii) Excretion of dhatus through urine along with ojus. This is asadhya.

II 1) sahaja3

2) Apathya nimittaja

1) Sahaja:- Charaka, Susruta, vagbhata & other authors mentioned this type. Sahaja

madhumeha is due to beejadosha and was mentioned as Kulajavikaras by charaka.

According to ayurveda sahaja madhumeha effects the persons from birthitself and is

asadhya.

2) Apathyanimittaja: This is due to indulgence in Apathyakara ahara and vihara. This

type was mentioned by almost all acharyas of Ayurveda. Apathyanimittaja

Madhumeha is sadhya/yapya if it is associated with other doshas i.e., kapha or pitta

along with vata.

III

1) Madhumeha due to vata associated with kapha.

2) Madhumeha due to vata associated with pitta4(ch-chi 6/34) while prescribing

kashyayoga to pramehas according to dosha, charka mentioned that for

vatajapramehas medicated taila and ghrita prepared drug of kaphaja and pittaja

pramehahara kashyayoga should be given according to associated dosha.

IV

1) Madhumeha:- as one of the 4 varieties of vatajamehas

2) Madhumeha as complications of other mehas if not treated properly. This type was

considered asadhya6. (A.H.Ni 10/2/2, Su.Ni chap 6)

V

1) Sadhya / Yapya

2) Kastasadhya

3) Asadhya

1) Sadhya/Yapya

i) Madhumeha due to vata associated with other doshas

ii) madhumeha due to gradual aggravation of vata

iii) madhumeha due to apathyakara aharavihara i.e., apathyanimittaja


Classification

4

2) Kastasadhya

i) Doshavritajanya

3) Asadhya

i) Madhumeha due to beejadosha

ii) Madhumeha as a complication of other mehas which were not treated properly.

iii) Dhatukshayajanya

iv) Madhumeha due to vata that is aggravated from the beginning

VI

1) Stula

2) Krisa7 (ch. Chi. 6/15)

This is given by charaka basing on the line of treatment. For stulapatient, sodhana

therapy was prescribed which includes vamana, virechana and vasti .For krisapatient

samsamana therapy was prescribed as they cannot tolerate sodhana therapy.

Constitutional variation also come with specific hetu i.e., sahaja and Apathyanimihaja

Madhumeharogi due to beejadosha is lean and madhumeharogi due to

apathyarimittaja vihara is obese.


Classification

5

Classification8

A. Clinicalclasses

Insulin dependent – Type – I

Noninsulin dependent – Type – II

a) nonobese

b) obese

Malnutrition related

Diabetes Mellitus associated with certain Conditions and syndromes

1) Pancreatic disease

2) Harmonal disease

3) Drug or chemical induced

4) Insulin or insulin receptor abnormalities

5) Genetic syndromes

6) Miscellaneous

Impaired glucose tolerance

a) Nonobese

b) Obese

c) Associated with certain conditions & syndromes

Gestational diabetes

B. Statistical Risk classes (normal glucose tolerance with substantially increased risk of

developing diabetes)

Previous abnormality of glucose tolerance

Potential abnormality of glucose tolerance.


Classification

6

References:-

1.CHA.CHI 6/9-12

A.H.NI 10/8-27

A.S.NI 10

SU.NI 6/18

CHA.NI 4/15-38

2.A.H.NI 10/21

3.CHA.CHI 6/57

4.CHA.CHI 6/52

5.CHA.CHI 6/34

6.A.H.NI 10/21

SU.NI CHAP 6

7.CHA.CHI 6/15

8.MALIN’S CLINICAL DIABETES


Samprapti

1

SAMPRAPTI

Samprapti is a process by which dosha dushyasamsarga will takes place and finally

manifests the disease. It includes the vaishamya of dosha, dushya, agni, srotas.

According to susruta, too much indulgence in the eliological factors relate to prameha

results into aparipakva vata, pitta, kapha and meda, which further proceed through

the mutravahasrotas to get localized in the vastimukha this leading to disease prameha

Vagbhata described two types of pathogenisis of Madhumeha i.e dhatuhkshayajanya

and doshavaranajanya3

Charaka has explained the samprapti in detailed manner it may be explained on the

basis of shatkriyakalas. The samanya samprapti process commences from the

nidanasevana

1) Sanchaya – the excessive indulgence in nidanasevana of guru, snigdhaahara and

avyayamadivihara leads to kaphadoshasanchaya having the quality of bahudravatha,

sanchayam occurs.

2) Prakopa – the bahudravatva kapha is prone to develop madhumeha and it is already

presnt in excess quantity from the beginning hence it gets aggravated rapidly when

the anukulanidana in there

3) Prasara – In this stage, the provoked Kapha gets spread all over the body owing to

sharirshaithilya. sharirashaithilya being one of the anukula factors for the nidana

towards dosha.

4) Sthanasamshraya – vikrita kapha has affinity towards bahu abadda meda due to their

similar properties and gets lodged there. Vikrita kapha after combining with

bahuabaddameda causes its vitiation. The other important dushyas are sharirakleda

and mamsa which are already increased in quantity prior to vitiation of kapha. The

provoked kapha with vitiated meda gets combined with sharirakleda or mamsa or

both. This is an important stage because the prodromal symptoms of the disease are

manifested in this stage.

5) vyakta – In this stage, two types of manifestation will occur

1) putimamsa pidaka due to mamsadhatu vitiation. 2) Mutravaha srotodusti due to

sharerakledadusti.


Samprapti

2

6) Bheda – In this stage various complications of the disease manifest and the disease

progress towards asadhya

Sampraptighataka of madhumeha:

Dosha : Sleshma pradhana tridosha sleshma is the main dosha responsible for Madhumeha

inspite of the fact that madhumeha is a tridoshajanyavyadhi. The other doshas like vata&

pitta only trigger off this samprapti and associate as anubandha.

Dushya : Rasa, Rakta, Mamsa, Meda, Majja, Sukra Vasa, lasika, ojus, kleda and according

to vagbhata, sweda

Srotodusti : The srotodusti laxana occur as sanga of kapha leading to vimargagamana and

atipravritti of kleda through the mootra.

Agni : Vaishamya of all agnis (or dhatvagnimandya)

Ama : Medogata ama produced due to jataragni mandhya and dhatvagnimadhya.

Adhistana : vasti

Udbhavasthana : Amasaya

Bhedavastha : Occurance of upadravas such as puti mamsa,pidaka etc.

Nature : chirakari, anusangi5

Dosha - All the three doshas are responsible for manifestation of madhumeha.

1) Kapha: It plays a dominant role in the samanya samprapti of madhumeha. It is the

first dosha to get vitiated . Acharya charaka while describing the causative factors

used the term kaphakriccha sarvam in it. It indicates the significance of this

doshadusti in prameha

2) Pitta: Here in avaranajanya madhumeha mainly the symptoms manifest because of

vriddi of pittadosha6. Pitta is in Kshaya avastha as compared to vata in vatajaprameha

samprapti .so Kshayalakshana of kapha and pittadosha may manifest in kshayajanya

madhumeha.7

3) Vata : This is the primedosha in the pathogenesis of madhumeha. Here vata gets

vitiated either because of its own etiological factors or because of avarana caused by

kapha, pitta and meda. This provoked vata carries vasa, majja, ojus towards vasti and

excretes them outside through urine resulting in depletion of dhatus, thus due to


Samprapti

3

severe depletion of dhatus, the symptoms manifest are karshya, dourbalya,

angasuptata, parisaranashila nature.

In susrutha samhita it is described that vyana and apana are the main culprits in prameha

thus in all the samprapti of prameha vyana acts as gatherer of kleda and apana as excretor.

The function of apanavayu gets aggravated resulting excretion of vital dhatus through the

urine outside the body8

B) Dushya:-

1) Rasa: Rasa is the seat of kapha and at the sometime it is the mala of rasadhatu. The

symptoms like alasya, gurutwa, karshya, klaibya etc. are produced as a result of

rasadusti.

2) Rakta: It mainly gets aggravated in pittajaprameha. The raktadusti laxanas are daha

visarpa, pidaka, dadru are produced as a result of Raktadusti9.

3) Mamsa: Mamsa and Kapha are having the same qualities. when kapha gets vitiated

mamsa looses its normal consistancy and develops shaithilya and provides space in

between for the accretion of morbid matter. This consequently result into

putimamsapidaka “ mamsaleshu avakasheshu “10

4) Meda: It is the dominant doosya in all types of prameha. kapha and meda have

close resemblance as they have same qualities.

In Madhumeha vitiation of medas results in two ways.

Abadhtha (asamhata) (qualitative) :- Normal function of medas is to produce

unctuousness in the body along with dridatva. so this abadhatva causes derangement

in the structure of meda produing shaithilya in the body.

Bahu (Qualitative) – Here in the pathogenesis meda is in excess quantity. This

medodhatu is aparipakva (ama)11

5) Majja: Due to vataprakopa kshaya of majjadhatu occurs. Thus vitiated majja

produced symptoms like netragaurava, angagaurava in madhumeha

6) Sukra: Sukradhatu gets affected in the pathogenesis of prameha, which is due to its

vitiation produces symptoms like dourbalya & kricchavyavayata. vata causes

depletion of shukra dhatu and also sukrameha.

7) Vasa: It is an upadhatu of mamsa and is sleshmika in character. The provoked vata

draws vasa towards vasti and exerts it through urine in the form of sneha.


Samprapti

4

8) Lasika : The aggravated vata proples lasika towards the vasti and then excretes it

through urine leading to increased micutition. Lasika is described as a dushya in

hastimeha.

9) Ojus: ojus is an important dusya in the samprapti of madhumeha. Here aggravated

vata transform the madhuratwa of ojus into kashayatwa and carries ojus towards vasti

and excretes through unine leading to ojokshaya

10) Kleda: it is also an important dusya after medas. In the samprapt,i kledadusti is in the

form of vriddi and not the kshaya. Hence bahukleda is manifest as prabhuta mutrata

and avilamutrata13 .


Samprapti

5

Pathogenesis of IDDM:14

Pathogenesis begins with genetic susceptibility to disease, with the destruction of islet

Beta cells of pancreas almost due to autoimmune process.

viralinfetion is a triggering factor but noninfectious agents may also be involved.

Autoimmune attack then follows.

The islet betacells become infiltrated by macrophages and activated cytotoxic T cells.

The infiltration usually called insulitis. Multiple antibodies against beta cells antigens

are present in the blood.

An autoimmune DM can develop in the absence of an environmental trigger i.e can be

purely genetic. Usually however the pathogenetic sequence is

Genetic predisposition

Environmental insult

Autoimmune destruction of Betacells

Diabetes mellitus (IDDM)

Destruction of Beta cells and development of IDDM:

The loss of insulin reserve occurs over a few to many years .The earliest sign of

abnormality is the development of islet cell antibodies when the bloodsugar and

glucose tolerance are normal and when insulin rensponses to glucose load are intact.

Continued destruction of betacells then leads to insulin dependantstage and

propensity of ketoacidosis

The immunedirected destruction of beta cells probably involves both humoral & cell

mediated mechanisms. Betacells have a lowcapacity for freeradical destruction and are

especially vulnerable to oxygen toxicity.


Samprapti

6

Pathogenesis of NIDDM:–

NIDDM is more common than IDDM. Its pathogenesis is less well understood. The

relation between the betacells abnormality and insulin resistance is not resolved. The

major environmental factor is obesity.

Both betacell defects and insulin resistances are present in the overt disease, which

more commonly exhibits familial aggregation, patients with type2DM have two

psychological defects Viz. abnormal insulin secretion and resistance to insulin action

in target tissues.

Insulin secretory defect and insulin resistance are both required for DM to be

expressed since massively obese person with marked insulin resistance may have

normal glucose tolerance. Presumably the Betacell lesion is not present in such

persons. This fact suggests that the primary defect resides in the insulin producing

cells.

Betacell mass is intact in type NIDDM in contrast with the situation in TypeI IDDM.

The alfa cell population is increased resulting in an elevated ratio of a Alfa to Beta

cells and an excess of glucagon relative to insulin that characterizes all hyperglycemic

states including NIDDM


Samprapti

7

Samprapti

1.

Sahaja Apathyanimittaja

Beejadosha Incompatible diet and activitiesEx: Mahasana, Ayrogyasana

diwaswapna etc

Sukra dosha Arthavadosha

Vatapradhana Tridosha

KaphaPittaVasaLasikaOjusmajja

ShareerakledaSukraMedasMamsaRasarakta

Vasti

Vataja Madhumeha

Prabhoota mutrata Avila/Madhurya mutrata


Samprapti

8

2.

Chronicityof other mehas ExcessiveRukhagunaof vata Eleminationof dhatus throughurine

Excessivedhatukshaya

Aggravationof vataPradhanatridosha

VatajaMadhumehaAvaranaof vatabydoshan

References:-

1.CHA.NI 4/5

2 CHA.NI 4/8

3.CHA.NI 4/11

4.CHA.CHI 6/4

5.SU.NI 6/4

6.SU.NI 6/9

7.A.H.NI 1O/8

8.A.H.NI 10/20,21

9.A.H.SHAREERA 3/6

10.CHA.SU 27/8,9,10

11.CHA.SU 26/61,62

12.A.H.NI 10/18

13.CHA.CHI 6/7

14.Harrison’s principles of internal medicine vol 1&2 14th edition 1998.


1

UPADRAVAS&

ARISHTALAKSHNASAccording to vagbhata all pramehas if not properly treated ultimately develop into

Madhumeha. Therefore it is to be understood that the upadaravas of pramehas are also the

upadravas of Madhumeha. However susrutsa and Vagbhata. have mentioned upadravas

separately for each doshaja group.

The general complications of prameha according to charaka as follows .1

1) Trishna 2) Atisara 3) Jwara

4) Daha 5) Dourbalya 6) Arochaka

7) Avipaka 8) putimamsa 9) Pidaka

10) Alaji 11) Vidradhi

Updravas mentioned in general by Basavaraju.

1) Aruchi 2) Angamardha 3) Trushna

4) Kasa 5) Bhrama 6) Shoda

7) Pidaka 8) Kandu

Updravas mentioned according to dosha by various authors (2,3)

kaphaja Pittaja Vataja

Makshikopasarpanam Vrishanayoravadaranam Hritgraham

Alashyam Vastibhedham Lohata

Mamsopachaya Medhratoda Anidra

Pratishyaya Amlika Kampa

Saidhilyam Atisara Shoola

Arochakam Jwara Badda purishatvam

Avipaka Arochaka Shosha

Kaphapraseka Vamadhu Udavartha

Chardi Paridhumayanam Swasa


2

Nidra Daha Kasa

Kasa Murcha

Peenasa Nidranasa

Panduroga

Peeta vitmootranetrata

Trishna

Vidbheda

Vagbhata added the following vatajaprameha upadravas more than susrta.

1) Kantagraham 2) Kasa

3) Shosha 4) Swasa

Charaka, vagbhata and the other author mentioned prameha pidaka but susruta coined them

as madhumeha pidaka and allotted an individual chapter for the treatment of these

Madhumeha pidaka but both are same. These will develop as a complication to particular

prameha was manifested.

Prameha pidaka mentioned by different acharyas 4,5,6

S.No. Charaka Susruta Vagbhata Bhoja

1) Sharavika Sharavika Sharavika Sharavika

2) Kacchapika Kacchapika Kacchapika Kacchapika

3) Jalini Jalini Jalini Jalini

4) Sarshapika Sarshapika Sarshapika Sarshapika

5) Alaji Alaji Alaji Alaji

6) Vinata Vinata Vinata -


3

7) Vidradhi Vidradhi Vidradhi Vidradhi

8) Masurika Masurika Masurika

9) Putrini Putrini Putrini

10) Vidarika Vidarika Vidarika

These pidakas may develop even in the absence of prameha due to dushta medas

(A.H.Ni 10/36)

Prognosis of Prameha Pidaka: 7

Sharavika

kacchapika

Jalini

putrini

vidarika

These are with unbearable pain and develop on more fatty areas

Vinata

Alaji

Masurika

Sharshapika

Vidhradhi

These are bearable and develops on less fatty areas

Charaka and Bhavamisra mentioned upadravas of pramehapidaka (Ch.17/109)

1) Trishna 2) Kasa

3) Mamasa sankocha 4) Moha

5) Hikka 6) Mada

7) Jwara 8) Visarpa

9) Mamsa arbuda

Prameha pidaka developed on guda, Hridaya, siras, Amsa, prusta, and Marma

pradesha along with other upadrava to a patient with durbhalagni are incurable.


4

UPADRAVAS

1) Trishna8 -due to excessive loss of kleda through mootra. pitta with its ushnaguna is

the maindosha here9.

2) Atisara - The longstanding vitiation of vata affects its sthana that is pakwasaya which

inturn causes atisara.

3) Paridhupana/daha - Manifest in kara and pada or sarvanga It is a pittaja nanatmaja

vikara and is described as saravanga dahanamiva santapa10

4) Jwara - Mainly due to pittapradhanya. Here as a result of dhatukshaya and reduced

vyadhikshamatva, jwara develops.

5) Dourbalya - It is because of dhatvagnimandya which later results in ojokshaya, leads

to dourbalya

6) Arochaka - Maindosha involved is kapha but pitta also causes arochaka.

7) Avipaka - is the ajeerna occurring as a result of agnimandhya by kapha

8) Pootimamsapidaka11,12 - These pidakas manifest due to vitiation of mamsa, meda

sonita with increased kleda result in development of pidakas, which develop shonita

resulting in pooyavidhradhi.

9) Bhrama- mainly due to pitta or vata or both and due to Rajodosha of Manas . This

upadrava produced where gambhira dhatus like majja are involved13.

10) Tama14- This develops during the terminalstage leading to death

11) Shoola - due to vata along with majja involvement15. Udarashoola due to

baddapurisha and udavarta.

12) Kandu16 – due to kapha which has attained bahudrava avastha and due to excess

sweda as a result of dusta medas

13) Alasya – due to kapha and meda

14) Pratisyaya17 – due to kapha, vata and ojokshya & pranavaha sroto dusti

15) Shaithilya 18– The dhathukshaya leads to anibada samyogata (loss of compactness)

16) Kaphapraseka – means excess lalasrava due to kaphabahudrava.

17) Mamsopachaya19 – Characterized by mamsasanghata due to mamsapradosha

18) Makshikopasarpana20 – this condition is the result of Tanumadhuryata and

subsequent madhura bhava of sweda .


5

19) Nidra – due to kapha dusti and Tamoguna .

20) Kasa & Swasa – are result of pranavaha srotodusti by vriddha kapha & vata.

21) Vrushanaavadharana – it may be result of kandu or kusta affecting vrishana

22) Vastibheda – due to vatadusti

23) Loulya – due to vyadhi prabhava and dhatukshaya.

24) Shosha – occurs due to dhatukshaya and vataprakopa.

25) Angamarda21 – udvestanamiva vedana due to vyanavatadusti

References:

1.CHA.NI 4/42

2.SU.NI 6/133.A.H.NI 10/224.CHA.SU 17/81-825.SU.NI 6/146.A.H.NI 10/25-267.CH.SU 17/102-1048.SU.NI 6/139.CHA.NI 4/4210.SU.NI 6/1311.CHA.NI 4/4212.SU.NI 6/1613.CHA.NI 4/3914.SU.NI 6/17,18,1915.CHA.CHI 6/716.A.H.NI 10/1817.SU.NI 6/1618.CH.NI 4/3219.SU.NI 6/1320.SU.NI 6/21


6

Complications of Diabetes mellitus

The complications of Diabetes mellitus can be acute or chronic. Acute complications are the

medical emergency and need immediate medical management, other wise the patient may go

into coma and ultimately death may occur among the acute complications, hypoglycemia is

the most serious one.

They can be classified as follows:

I) Acute metabolic complications:

i) Diabetic ketoacidosis

ii) Hyperosmolar coma

ii) Hypoglycemia

II) Chronic complications:

A) Angiopathic complications

i) Microangiopathic – Retinopathy, cataract, glaucoma, Nephropathy,

neuropathy

ii) Macroangiopathic - coronary arterydisease, cerebrovascular disease

B) Infections: Skin infections, pulmonary koch’s, urinary tract infections,

vaginal candidiasis, gangrene of feet etc.

Others – Gastroparesis, diarrhoea, sexual dysfunction.

Diabetic neuropathy occurs in approximately 50% of individuals with longstanding

type-1 and Type-2 DM.

Diabetic peripheral neuropathy presents with distal sensoryloss, hyperesthesia,

paresthesia & pain also occurs.

Diabetics have increased susceptibility to various infections such as tuberculosis,

pneumonia, pyelonephritis, carbuncles and diabeticulcers.

Diabetic ketoacidosis(DKA):-

DKA accounted for over40 percent of diabeticdeaths in the preinsulin era. A number

of patients are already ketotic when diagnosed. Skipping injections of insulin is an

Important antecedent.


7

The clinicalpicture of DKA gradually develops over a period of 18hours to 3days.

There is a marked increase in polyuria,thirst,weakness and painful musclecramps

Rapid deep and kussumal breathing is evident with increase in acidosis. Lethargy and

drowsiness are followed by clouding of conciousness and confusionalstate

Diabetic retinopathy:-

Retinopathy is one of the major riskfactors of DM. The incidence of blindness or poor

vision is 20times more common in diabetic than in nondiabetics

Visual symptoms do not appear until late in the course of retinopathy.Excess of

exudates,oedema or ischemia affecting the maculararea is a common cause of

visualloss in NIDDM

Preproliferative retinopathy is more common in IDDM. This stage is heralded by the

appearance of multiple cottonwool patches resulting from microinfarcts.

Diabetic nephropathy:-

DN is a specific form of renaldisease. A major cause of death ,disability among

diabetics,it accounts for 25-40percent of all cases with end stage renalfailure(ESRF)

Symptoms arise late in the course of nephropathy. Heavy proteinuria leads to

oedema,hypoalbuminaemia and hypertension seen in 15-25percent.

Diabetic neuropathy:-

Peripheral neuropathy is the commonest among longterm complications ofdiabetes.

Paraesthesia such as tingling,burning,numbness,coldareas,aches and pains may be the

presenting symptoms of around 30 percent of patients


Sadhya Sadhyata

1

SADHYA SADHYATA&

SAPEKSHA NIDANA

Acharyas mentioned prognosis of prameha according to dosha.

1) Kaphajaprameha – Sadhya – due to Samakriya

2) Pittajaprameha – yapya – due to vishamakriya

3) vatajaprameha – Asadhya – due to virudhopakramata

Prameha with tulyadhushyata was mentioned as sukhasadhya i.e., easily curable

The four types of vataja pramehas are incurable owing to their great atyayikata

(emergency) and the autogonism involved in the treatment

According to Vagbhata kaphaja prameha has if not treated gradually convert into

pittaijaprameha and the both of may transform into vatajaprameha3

1) Sadhya / Yapya Vatajamehas 4

i) vatajamehas associated with either kapha or pitta

ii) vatajameha. Due to gradual and secondary aggravation

2) Kastasadhya – Doshavrutajanya 5Ch.Chi 6/13)

3) Asadhya

i) Dhatukshayajanya 6

ii) Kulaja – Madhumeha due to beejadosha

iii)vatajameha / Madhumeha

iv) Madhumeha with all poorvaroopas from earlystage.

v) Madhumeha as a complication of other mehas that are untreated.

vi) vatajameha / Madhumeha in which urine is syava and aruna varna

If the disease is developed due to vitiation of one dosha and the duration is less than

one year, the disease is curable. If two doshas are involved, the disease can be


Sadhya Sadhyata

2

controlled. If 3 or moredoshas are involved and associated with any group of

complications is considered incurable.

According to susruta and vagbhata, madhumeha is itself a complication and it is a fact

that madhumeha is a sannipata disease.

References:-

1.CHA.NI 4/34

2.SU.NI 6/8

3.A.H.NI 10/41

4.CHA.CHI 6/13

5.CHA.CHI 6/13

6. A.H.NI 10/21


CHIKITSA&

PATHYAAPATHYAKRAMA

In general chikitsa is the method adopted for eradication of the disease from the body.

The aim of treatment is to restore swasthya. That means to normal functions of agni,

dhatu, mala and maintain mental health. The primary importance of chikista lies in

samprapti vighatana.

General schedule of treatment of Prameha according to Dosha:-

Dosha Name of the Therapy

Kaphaja Prameha Samsodhana, lekhana, langhana,

Apatarpana

Pittaja Prameha Virechana, Santarpana, Samsamana

Vataja prameha 1. If associated with Kapha, taila

prepared from decoction of

kaphaja pramehahara drugs

should be given

2. If associated with pitta ghrita

prepared from decoction of

pittaja pramehahara drugs

should be given.

Charaka classified patients of prameha into two categories for treatment purpose.1(cha.chi. 6/15 – 17& 18)

1. Stula – Samsodhana therapy was prescribed.

2. Krisha – Brumhana & Samsamana therapy was prescribed.

.

While classifying the drugs susruta has given the following groups as useful in prameha2(su.sutra 38 & 71,72,73)

1. Aragvadadi gana

2. Salasaradigana

3. Mushakadigana


4. Triphala

5. Trikatu

6. Trapvadigana

Since the pramehas are caused mainly because of the vitiation of Kaphadosha and the

corruption of the medodhatu, the following groups of drugs which are stated to restore the

normalcy of kapha and medas, may be used.

1. Salasaradigana

2. Varunadigana

3. Lodhradigana

4. Ushakadigana

5. Arkadigana

The samsodhana kriya vamana, langhana adopted at appropriate times to cure

kaphaprameha.

The virechana kriya, Santarpana kriya, samanakriya cure pittajameha 3(cha.chi.6/23)

After the sodhanakarma is completed the patient is to be subjected to santrapanakriya,

although the prameha is a santarpanajanya roga, the patient should not be subjected

to apatarpanakriya,because it may result in gulma,kshaya,suppression of urine.. The

santarpanakriya should be carried out considering the strength of the agnibala.4(cha.chi.6/15)

A krisha or emaciated patient who is not capable of with standing the purificatory

procedures requires Brimhana kriya 5(cha.chi 6/15)

The following oils may be used for snehakarma for a stula

prameha.

1. Oil prepared with sarshapa, arista, Nikumbha and karanja.

2. Trikantaka taila.

A ghrita prepared out of Priyangvadigana drugs is to be used for vamanakriya. After

samasarjanakriya is over, the patient is subjected to virechanakriya with appropriate

dravyas. (su.chi.11/72)


Importance of Apatarpana:-

Because of involvement of bahu and abadda mamsa & medas and dravarupa sleshma,

apatarpana therapy was preferred.

Importance of internal administration of oil in vatajameha:-

1. Charaka mentioned administration of taila and ghrita according to associated

dosha for the treatment of vataja mehas (cha.chi. 6/35)

2. According to Astanga Hridaya chikitsa8, 12/9–10 “Vatolbaneshu snehamscha

Prameheshu Prakalpayeth” For treatment of vataja prameha, internal

administration of oils prepared from kaphaja and pittajapramehahara drugs was

advised.

3. In Bhavaprakasha madhyamakanda, pramehaadhikaara internal administration of

snehas in vatajamehas is advised. “Vatolbaneshu meheshu snehapanam

visheshatah”. snehas prescribed in Bhavaprakasha.

1. Dadimadhya ghritam.

2. Dhanvantaram ghritam & tailam.

Snehas prescribed in Yogaratnakaram

1. Simhamrutha ghritam.

2. Haridradi tail

Samanachikista:-

Samanachikista is indicated for a prameha patient who is fit and completed successfully the

sodhanakarma and also who is not fit for sodhanakarma.


TREATMENT 9

A) Goals of treatment of Diabetes:-

Diabetes mellitus requires on going medical care as well as patient & family

education both to prevent acute illness and to reduce the risk of long-term complications. The

therapeutic objective is to restore known metabolic derangements towards normal in order to

prevent and delay progression of diabetic complications. The aims of treatment have been

varied according to an arbitrary division of patients into three categories ranging from those

in whom symptomatic relief done seems the most appropriate or any attainable goal to those

in whom an attempt at maximal prophylaxis against future tissue damage seems desirable &

possible.

B) Treatment regimens:-

i) Diet:- A well balanced nutritious diet remains a fundamental element of therapy. In

obese patient with mild hyperglycemia the major goal of diet therapy in weight reduction by

caloric restriction.

1. Intake of protein and carbohydrate according to the recommendation of American

Diabetic Association.

2. Dietary fibres:- Food such as oatmeal, cereals and beans with relatively high soluble

fibre content as staple component of the diet in Diabetes. These tend to retard nutrient

absorption rates so that glucose absorption is slower and hyperglycemia may be

slightly diminished. High soulbe fibre content in the diet may also have favourable

effect on blood cholesterol levels.

3. Artificial sweetners:- Diabetes can use artificial sweetners like aspartame, sucralose,

acesulfame.

ii) Oral anti diabetic agents:- Oral drugs are used to lower blood

glucose level by achieving following goals.

1. Drugs that primarily stimulate insulin secretion.

2. Drugs that after insulin action.

3. Drugs that principally affect absorption of glucose.


a) Sulfonylureas:-

Mode of Action:- Stimulate production of insulin by increasing number of insulin

receptors.

Indication:-

1. Maturity onset diabetes of average weight not controlled by diet.

2. Diabetes or normal weight stabilized on insulin dosage not more than 30 units per day

who have never been ketotic.

3. Failure to lose weight when this is indicated.

Contra indication:-

1. Juvenile diabetes

2. Patients with ketosis

3. Obese adult onset uncontrolled diabetes.

4. Insulin taking diabetics.

5. Presence of renal, hepatic or cardio respiratory disease or alcoholic abuse.

Adverse effects:-

1. Hypoglycemia

2. Dyspepsia

3. Skin rash

4. Facial flushing after ingestion of alcohol mostly ( chlorpropramide)

5. Cholestatic jaundice (chlorpropramide)

6. Blood dyscriasis

Drug interactions with Sulfonylureas:-

a) Increased hypoglycemic action:- –blockers, Sulphonamides

Phenyl butazone, chloramphenicol, Cyclophospamide.

b) Decreased hypoglycemic action:- Adrenergic compounds,

Corticosteriods, oestrogen containing oral contraceptives, thiazide

Diuretics, Phenytoin.

Biguanides:-

Mode of action:- Major effect is to increase peripheral uptake of glucose and in large doses

to delay or decrease intertinal absorption. Biguanides do not cause hypoglycemia.


Indication:-

1. Treatment of Maturity onset, diabetic who failed to lose weight on diet.

2. In Combination with Sulfonylureas – To enhance the inadequate or failing effects of

sulfonylureas.

3. As an adjunct to insulin therapy in brittle diabetes whose blood sugar tends to swing

unpredictably, one who is prone to ketosis and who develops hypoglycemia with only

slight overdose of insulin.

Adverse effects:-

1. Malaise, weakness, Drowsiness

2. Metallic taste in mouth, Anorexia, Nausea, dyspepsia, Diarrhoea

3. Lacticacidosis

iii) Insulin:-

Insulin is indicated for Type –1 diabetic as well as for Type–2 diabetic patients whose

hypoglycemia does not respond to diet therapy either alone or combined with oral

hypoglycemia drugs. Insulin injections are very much necessary in severe condition of

Hyperglycemia.

There are various preparations are present depending upon their purity, solubility &

species like( Human / Bovine)

Four Principle types of Insulins are available:-

1. Ultra –short acting with very rapid onset & short duration.

2. Short acting with rapid onset of action.

3. Intermediate acting.

4. Long action with slow onset of action.

The injection can be given with the help of syringes with half inched ultra fine needles

attached available in 1ml, 0.5ml, 0.25ml sizes.

For the injection any part of the body covered by loose skin can be

used such as abdomen, thigh, upperarms, flanks & upper buttocks.

iv) Insulin like growth factor –1 (IGF –I) therapy

v) Aspirin therapy.

* * * * *


References:-

1. CHA.CHI- 6/15-17&18

2. SU.SUTRA- 38/71,72,73

3.CHA.CHI- 6/23

4.CHA.CHI- 6/15

5.CHA.CHI- 6/15

6.SU.CHI- 11/62

7.CHA.CHI- 6/35

8.A.H.CHI- 12/9-10

9.MALINS CLINICAL DIABETES

10.CHA.CHI 6/46

11.CHA.CHI 6/20-22

12.CHA.CHI 6/39

13.CHA.CHI 6/42

14.CHA.CHI 6/46

15.SU.CHI 11/16

16.SU.CHI11/34

17.Dr.SHENOY,JOURNAL OF INDIANMEDICAL ASSOCIATION VOL.1


DRUG REVIEW

Drug plays a vital role in the management of the disease.Due to this reason, it had been

placed next to physician in the chatuspada.It has been well said by charaka is ‘a drug i.e

understood perfectly is comparable to poison,weapon, fire and thunderbolt’. While the

perfectly understood drug is comparable to ambrosia.

The best drug is that which cures the disease promptly and also preserves or

sustains the helath of an individual.

The drug selected for present clinical study on prameha is “SOMARAJYADI

CHURNAM”.

SOMARAJYADI CHURNAM:-

Somrajyadi churnam is anubhutayoga to prove its scientific efficacy. I selected

this yoga for trail.

It contains 4 ingredients. They are BAKUCHI,(Psoralea corylifolea)

AVARTHAKI,(Cassia auriculata) MADHUNASHINI, (Gymnema

sylvestris)SUNTI(Zingiber officinale). Most of the drug have tikta,

kashayarasa,laghu , rooksha guna, katuvipaka.These are said to be kaphagna,

mehagna, medogna.

Tikta, kashayarasa, laghu, rookshaguna produces rookshana effect and they are

having opposite qualities to that kapha and medas. Hence they act as mehagna and

kaphagna. When medas is reduced then the pressure on vapavahana is also

reduced as it is the moolastana of medovahasrotas.

Bahudravatva is present in madhumeha. Tikta, kashayarasa produces shoshana

effect and there by bahudravatva is reduced.When bahudravata reaching vasti

reduces then prabhootamootrata, pratyatmalaxana of prameha also reduces.Pipasa

which is depended on prabhootamootrata also reduces and there by somarajyadi

churnam checks the pathogenesis of madhumeha.


INGREDIANTS:-

1. Bakuchi – 1 part

2. Avarthaki – 1 part

3. Madhushini – 1 part

4. Sunti – 1 part


BAKUCHINomenclature of the drug:-

Latin name - Psoralea corylifolia

Family - Papillionaceae

Sanskrit - Bakuchi,Sugandhikantaka,Somaraji.

English - Babchi seeds

Telugu - Bavanchalu

Hindi - Babchi ,Bhavaj

Bengali - Latakantaki

Tamil - Karpokanethi

Persian - Vabkuchi

Synonyms:-

Bakuchi,Avalguja,Putiphala,Kustagni,Suparnika,Sisilekha,Kalameshi,Sita,Chanda

Parts used:-Seed,Seed oil

Pharmacodynamic principles of the drug:-

Rasa - katu ,tikta

Guna - Laghu,Rooksha

Veerya – Ushna

Vipaka -katu

Karmas:-

Dosha - Vatakapha samana

Dathu - Rasayana

Indications:-

Pramehahara,Madhumehahara,Mahakusta,Kshudra kusta

In Dhanvantari nighantu it is included in Guduchyadi varga.Charaka had included this

drug in Tiktaskanda.Susruta had included this drug in Katuvarga.


Chemical composition:- Seeds contain an unsaponifiable oil.Chief active principles Of

the seed is essential oil,resin,traces of substances of alkaloidal nature. Oil contian

psoralen,Bakuchiol,isopsoralen


MADHUNASHINI

Nomenclature of the drug:-

Latin name - Gymnema sylvestris

Family - Asclepiadaceae

Sanskrit - Ajagandhini, Anyada, Avarthini

Telugu - Podapatri

English - Periploka of the woods,Small Indian ipecauna

Hindi - Gurmar, Meshashringi

Urdu - Kakashing

Gujarathi - Dhuleti

Bombay - Kavali, Wakandi

Marati - Bedaki, Kalikardori

Synonyms:-

Vishani, Ajashringika, Meshashringi ,Sarpadarustrika

Parts used:-

Leaves, root


Rasa - Kashaya,Tikta

Guna - Laghu,rooksha

Veerya _ Ushna

Vipaka - Katu

Karma:-

Kaphavata shamaka, Sodhakara, Vedanahara ,Kaphagna, Mootrala.

Indication:-

Prameha. Kusta, Kasa, Krimi


Chemical composition:-

Sundried leaves contain two resins, the resin insoluble in alcohol., the resin soluble in

alcohol

Calcium oxalate

Pararabin

Glucose

Carbohydrates

Tartaric acid

Gymnemic acid

Leaves on oral administration increased insulin levels in Alloxan rats(Pharmacological

research communication 1981)


AVARTHAKI

Nomenclature of the drug:-

Latin name - Cassia auriculata

Family - Caesalpinaceae

Sanskrit - Avarthaki

English - Mature tea tree,Tanners cassea

Telugu - Tangedu

Hindi - Tarvar

Gujarath - Awal

Maharastra - Taraveda

Bengal - Tarwal

Malayalam - Aveeram

Synonyms:-

Avarthaki, Charmaranga, Peetakalaka, Mayahari

Parts used:- Pulp,Root bark, Flowera, Leaves, Root


Rasa - Kashaya, tikta

Guna - Laghu, rooksha

Veerya - Seeta

Vipaka - Katu

Karma:-

Kapha pittahara,Tridoshagna,Stambhani,Vrishya

Indications:-

Prameha, Vrana,Natrabhishyanda,Atisara


Chemical composition:-

Fruit contains dark yellow volatile oil with honey like odour. Pulp contains sugar,gum,

astringent matter,gluten


SUNTI

Sunti is dried form of ardhraka.

Nomenclature of the drug :-

Latin name :- Gingiber officinale.

Family :- Gingideraceae

Sanskrit :- Nagara

Telugu :- Sunti

English :- Ginger

German :- Inguuer

Urdu :- Ardhraka

French :- Gingembre

Panjab :- Ada

Malayalam :- Andrakam

Synonyms:-

Ardhraka , Shringavera, Katubadhra, Katukam, Katushringi, Katutoya, Visvabheshajam.

Parts Used:- Rhizome


Rasa – Katu

Guna – Laghu, Guru

Veerya – Seeta

Vipaka – Madhura

Karmas:

Kaphavataharam, Deepana, pachana, vrishya,swaryam, jihwakantavishodanam.

Indications:-

Prameha, Amavata, Sopha, Gulma


Gana:- Charaka included in deepaniya, triptigna, arshogna, stanyashodhana, soolagna,

trishnanigraha, sirovirechana.

Pippalyadi, triktatu(susruta).

Chemical Composition:-

Contains an aromatic, volatile oil.

Camphene, phalladrene, zingeberene.

Cineol, gingerol, oleoresin, gingerin.

K-oxalate.


1

Materials and methods

My dissertation entitled “A CLINICAL STUDY ON THE EFFECT OF SOMARAJYADI

CHURNAM IN THE MANAGEMENT OF PRAMEHA “ was carried out on 40 patients

who attended the OP and IP sections of Govt.Ayurvedic college/Hospital, Erragadda.

HYD.during Jan 2007 to sep2007.

Aim of study:-

1.To evaluate the effect of “SOMARAJYADI CHURNAM”in patients suffering from stula

and krisha Madhumeha.

2.To evaluate the effect of Somarajyadi churnam in NIDDM patients.

3.Comprehensive literary study on prameha.

1.Materials:-

1. patients

2. drugs

1. Patients :- 40 patients were taken for the study.

2. Drugs:- Somarajyadi churnam with sukoshna jalam

2. Methods:-

1.Location of study:- For the purpose of clinical trials 40 patients were selected from OP and

IP department of Kayachikitsa of Dr.B.R.K.R Govt.Ayurvedic college/

hospital,Erragadda,Hyderabad.

2.Selection of patients:- 40 patients of different age groups were selected on the basis of

FBS&PLBSand corresponding urine sugars.

Diagnostic criteria:-

Criteria - 1:- patients presenting with pratyatma lakshana of Madhumeha –prabhoota and

avilamootrata with mootra or tanumadhuryata with or without roopa are taken as

Madhumehi.


2

Criteria -2:-

FBS -80 -120mg/dl

PLBS -140 -180mg/dl

Inclusion criteria:- patients fulfilling the following conditions were included.

1. patients between 30yrs -70yrs.

2. Stula and krisha Madhumehi.

3. Patients with Type 2DM with FBS greater than 120mg/dl and lesser than 180mg/dl

and PLBS of more than 160mg/dl and less than 300mg/dl.

Exclusion criteria:- The following patients were excluded from the study.

1.patients below 30yrs.

2.Jatapramehi

3.IDDM patients

4.Gestational diabetes

5.DM secondary to drugs like corticosteroids or due to secondary disorders

Investigations:-The following investigations were done on a mandatory basis.

1.FBS

2. PLBS

3.Urine sugar

Research design:-

A single blind clinical trail with pre and post test design was adopted.

Intervention:-

Intervention was done with Somarajyadi churnam taken,the 4 drugs in equal parts and the

powder is given in 2 divided doses.i.e 6 grams in 2 doses with sukhoshnajalam before food.

Assessment Criteria:-

Any change in the following symptoms were noted and taken for assessment.


3

1.Fasting blood sugar

2.post prandial blood sugar

3.post prandial urine sugar

4.sweda adhikhya

=>Sweating after heavy work and fast movement -- 0

=> Profuse sweating after moderate work and movement --- 1

=>Sweating after little work and movement

(stepping ladder etc…) ----2

=>Profuse sweating after little work and little movement ----3

=>Sweating even at rest or cold weather ----4

5.Prabhoota mootrata(quantity & in litres)

1.50 to 2.00 - 0

2.00 to 2.50 -1

2.5 to 3.00 -2

3.00 onwords.. -3

6. Avila mootrata(Turbid Urine)

Crystal clear fluid - 0

Failntly cloudy or smoky -1

Turbidity clearly present but newsprint easily

read through testtube -2

Newsprint not easily read through testtube -3

Newsprint cannot be seen through the testtube -4

7. Stoulya assessed according to body mass index in (Kg/H in m2)

Undernourished (<20) - 1

Normal weight (18.5 to 24.9) - 0

Overweight (25 to 29.9) -1

Obese(30 to 39) -2

Morbid obesity (40 & above) -3

8. Dourbalya

Can do routine exercise/work -0

Can do moderate exercise with hesitancy -1


4

Can do mild exercise only,with difficulty -2

Can’t do mild exercise too.. -3

9. Suptata (Numbness & Tingling sensation)

No Suptata - 0

Karapadatala Suptata in continuous - 1

Karapadatala Suptata in continuous

But not severe -2

Karapadatala Suptata in continuous & severe - 3

10.Daha(Burning sensation)

No daha --0

Karapadatala daha/supti in continuous – 1

Karapadatala daha/supti in continuous

But not severe –2

Karapadatala daha/supti in continuous & severe - 3

11.Bahvashita(polyphagia)

No Bahvashita as usual - 0

Slightly increased (1-2 meal) - 1

Moderately increased (3-4 meals) - 2

Markedly increased (5-6 meals) - 3

12.Trushna(Polydipsia)

Feeling of thirst 7-9 times/24 hours - 0

Feeling of thirst 9-11times/24 hours - 1

Feeling of thirst 11-13times/24 hours - 2

Feeling of thirst > 13times - 3


Observation

1

OBSERVATION1. Age Incidence

Age Group No of Pts %

31- 40 3 7.5%

41 – 50 12 30%

51- 60 20 50%

61-70 5 12.5%

31-40

41-50

51-60

61-70

2. Sex incidence

Sex No of Pts %

Male 26 65%

Female 14 35%

Male

Female


Observation

2

3. Marital Status

Status No of Pts %

Single 6 15%

Married 34 85%

6

34

0

5

10

15

20

25

30

35

Single Married

Marital Status

Series1

4. Religion Incidence

Religion No of Pts %

Hindu 31 77.5%

Muslim 4 10%

Christian 5 12.5%

Hindu

Muslim

Christian


Observation

3

5. Socioeconomic status

Status No of Pts %UP 0 0

P 5 12.5

LM 6 15

M 15 37.5

UM 10 25

R 4 10

0

56

15

10

4

0

2

4

6

8

10

12

14

16

UP P LM M UM R

Socioeconomic status

Series1

6. Incidence of Addictions

Habits No of Pts %Smoking 16 40

Tobacco 5 12.5

Alcohol 4 10

T/C 15 38.5

16

54

15

0

2

4

6

8

10

12

14

16

Smoking Tobacco Alcohol T/C

INCIDENCE OF ADDICTIONS

Series1


Observation

4

7. Dietary Habits

Diet No of Pts %

Veg 12 30

Mixed 28 70

Veg

Mixed

8. Deha prakriti

Prakruti No of Pts %

VP 6 15

PV 3 7.5

VK 14 35

KV 9 22.5

PK 3 7.5

KP 5 12.5

6

3

14

9

3

5

0

2

4

6

8

10

12

14

VP PV VK KV PK KP

DEHA PRAKRITI

Series1


Observation

5

9. Satva Incidence

Satvam No of Pts %

Pravara 4 10

Madhyama 26 65

Avara 10 25

Pravara

Madhyama

Avara

10. Status of Agni

Agni No of Pts %Teekshna 14 35

Sama 0 0

Vishama 15 37.5

Manda 11 27.5

14

0

15

11

0

2

4

6

8

10

12

14

16

Teekshna Sama Vishama Manda

STATUS OF AGNI

Series1


Observation

6

11. Bala Incidence

Bala No of Pts %

Pravara 8 20

Madhyama 26 65Avara 6 15

8

26

6

0

5

10

15

20

25

30

Pravara Madhyama Avara

BALA INCIDENCE

Series1

12. Family HistoryRelations No of Pts %

First Degree 18 45

Second degree 1 2.5

No familial history 21 52.5

First Degree

Second degree

No familial history


Observation

7

13. According to Chronicity

Age No of Pts %

Below 1 year 12 30

1 – 10 years 22 55

Above 10 years 6 15

12

22

6

0

5

10

15

20

25

Below 1 year 1 – 10 years Above 10years

ACCORDING TO CHRONICITY

Series1


Observation

8

Observations

In the present study, 40 patients suffering from prameha / Madhumeha, fulfilling the

inclusion criteria were registered. Following are the detailed descriptive statistical analysis of

the patients included in the study.

Observations:-1. Age Incidence: The majority of the patients (50%) were reported in the age groups of

51-60 years followed by 30% in the age groups of 41-50 years, 12.5% in the age

group of 61-70 years, 7.5% in the age group 31-40years.

2. Sex Incidence: The majority of the patients (65%) were males compared to females

(35%).

3. Marital Status Incidence: 85% of patients were married only 15% of patients were

unmarried.

4. Religion Incidence: Maximum number of patients i.e., 77.5% were Hindus, 12.5%

were Christians, 10% are Muslims.

5. Socioeconomic status: It is observed that maximum patients belongs to middle class

37.5%, upper middle class is 25%, lower middle class is 15% and rich were 10%.

6. Incidence of Addictions: Data depicts that maximum no of patients i.e., 40% were

smokers, Habit of tea/coffee is 38.5%, Tobacco chewing is 12.5% and addiction to

alcohol is 10%.

7. Incidence of Dietary Habits: 70% of the patients were accustomed to mixed type of

diet while 30% were vegetarians.

8. Incidence of Dehaprakriti: A majority of the patients are vatakapha (35%) followed

by 22.5% were Kaphavata, Kaphapitta 12.5%, vatapitta is 15%, Pittavata is 7.5%,

pittakapha is 7.5%

9. Incidence of Satva: Satva analysis of the patients revealed 65% of Madhyama satva,

25% avara, 10% pravara satva.


Observation

9

10. Incidence of agni: Vishamagni is seen in 37.5%, teekshnagni 35%, Mandagni in

27.5%.

11. Incidence of Family history: first degree family history is seen in 45% of the

patients, second degree family history is seen in 2.5%, no familial history in 52.5%.

12. Incidence of chronocity: 53% of the patients are having diabetes in 1-10 years, 30%

of the patients are below 1 year, 15% of the patients are above 10 years.


1

EFFECT OF THE TREATMENT :

The signs and symptoms recorded before the commencement of the treatment have beenreviewed finally at the end of the period of treatment in each case . The data of possessing thenumber of cases relieved, improved and unchanged. As regards to sign and symptom togetherwith the percentage are represented, the nearest round figures for the percentage were takeninto account to avoid fraction.

Effect of TreatmentNo. of Cases

SN Signs andSymptoms

Total No. ofCases Relieved % Improved % Unchanged %

1 Prabhootamutrata 32 26 81% 4 13% 2 6%

2 Avilamutrata 6 4 66% 1 17% 1 17%

3 Atitrishna 28 19 67% 3 10% 6 23%

4 Atikshudha 30 16 54% 7 24% 7 24%

5 Mutramadharyata 34 21 61% 8 23% 5 16%

6 Tanohmadhuryata 22 16 74% 3 13% 3 13%

7 Suptata 18 12 66% 2 11% 4 23%

8 Dourbalya 33 24 73% 3 9% 6 18%

9 Karapadadaha 25 20 80% 4 16% 1 4%

10 Musclecramps 17 6 35% 5 29% 6 36%

11 Atisweda 12 10 84% 1 8% 1 8%

12 Stoulya 4 1 25% 2 50% 1 25%


2

Statement showing the blood & urine sugar levels & Weight

Blood sugar beforetreatment

Blood sugar aftertreatment

Urine sugar beforetreatment

Urine sugar aftertreatment

S.No Regd No. FBS PLBS FBS PLBS FUS PLUS FUS PLUS

Weight beforetreatment

weight aftertreatment

1 15481 172 245 110 146 1% 2 Nil Nil 59 58

2 15523 142 228 98 172 0.5 2 Nil Trace 67 67

3 506 145 198 124 142 0.5 1 Nil Nil 48 48

4 16426 110 200 114 162 0.5 1 Nil Trace 68 69

5 18233 195 300 105 199 2 2.5 Nil 1 62 62

6 21498 142 247 112 168 1 2 Nil Trace 63 62

7 25253 106 230 96 136 0.5 1.5 Nil Nil 74 73

8 25894 190 280 160 210 1 1.5 Nil 0.5 62 60

9 26543 140 194 100 140 0.5 1 Nil Nil 58 59

10 26537 115 165 100 145 0.5 1 Nil Nil 44 43

11 28437 120 223 80 130 1 1.5 Nil Nil 62 62

12 29124 152 268 128 190 1 1 nil o.5 51 51

13 29431 270 380 270 370 2 2.5 2 2.5 63 62

14 42468 125 215 75 145 0.5 1 Nil Nil 72 72

15 2799 155 230 105 165 1 1.5 Nil Nil 41 41


3








16 3223 114 164 100 145 0.5 1 Nil 0.5 44 43

17 2723 140 300 118 174 0.5 2 Nil 1 64 64

18 2850 198 266 192 238 1 1.5 1 1.5 59 59

19 2797 145 205 114 156 0.5 1 Nil Nil 65 65

20 2798 166 222 88 142 1 1.5 Nil Trace 67 67

21 2853 118 192 108 177 0.5 1.5 Nil 1.5 55 54

22 2924 107 214 10 179 0.5 1.5 Nil 1 70 70

23 3056 141 215 140 215 0.5 1.5 0.5 1.5 79 79

24 2798 210 300 174 268 1.5 2 1.5 1.5 54 54

25 2622 230 294 106 157 1.5 2 Nil Trace 69 68

26 2597 258 305 202 305 2 2.5 2 2.5 57 57

27 2983 138 172 108 164 0.5 1 Nil 1 53 53

28 2384 155 235 98 148 1 1.5 Nil Nil 51 51


4








29 2788 142 198 78 128 1% 1.5 Nil N 75 74

30 2580 181 264 95 153 1 1.5 Nil Trace 63 63

31 2932 160 290 172 216 1.5 2 1 2 40 39

32 3542 166 242 110 174 1 1.5 Nil 0.5 58 58

33 3849 128 176 114 158 0.5 1 Nil Nil 66 66

34 4057 170 260 140 200 1 1.5 Nil 1 59 59

35 4358 180 290 120 210 1 2 Nil 1 49 50

36 4298 140 230 100 160 0.5 2 Nil 1.5 64 65

37 4178 154 202 140 146 0.5 2 Nil Nil 52 52

38 3078 168 240 114 160 1 2 Nil 1 48 48

39 3199 132 218 168 238 0.5 2 1 2 69 69

40 4050 144 200 174 213 0.5 1.5 1.5 2 57 57


Results

1

RESULTS TABLE

1. Effect on Prabhoota Mutruta

Mean

BT ATDifference in Means

1.875 1.538 0.337

1.875

1.538

0

0.5

1

1.5

2

Mean

BT AT

Effect on Prabhoota Mutruta

BT

AT


Results

2

2. Effect on Avilamutrata

Mean


1.5 1.25 0.25

1.5

1.25

1.1

1.15

1.2

1.25

1.3

1.35

1.4

1.45

1.5

Mean

BT AT

Effect on Avilamutrata

BTAT


Results

3

3. Effect on Atitrushna

Mean


1.286 1.158 0.128

1.286

1.158

1.081.1

1.121.141.161.181.2

1.221.241.261.281.3

Mean

BT AT

Effect on Atitrushna

BTAT


Results

4

4. Effect on Atikshudha

Mean


1.333 1.25 0.083

1.333

1.25

1.2

1.22

1.24

1.26

1.28

1.3

1.32

1.34

Mean

BT AT

Effect on Atikshudha

BTAT


Results

5

5. Effect on Karapadasuptata

Mean


1.444 1.167 0.277

1.444

1.167

0

0.2

0.4

0.6

0.8

1

1.2

1.4

1.6

Mean

BT AT

Effect on Karapadasuptata

BTAT


Results

6

6. Effect on Dourbalya

Mean


1.400 0.200 1.200

1.4

0.2

0

0.2

0.4

0.6

0.8

1

1.2

1.4

Mean

BT AT

Effect on Dourbalya

BTAT


Results

7

7. Effect on Karapadadaha

Mean


1.2 0.85 0.35

1.2

0.85

0

0.2

0.4

0.6

0.8

1

1.2

Mean

BT AT

Effect on Karapadadaha

BTAT


Results

8

8. Effect on Muscle Cramps

Mean


1.152 0.1 1.050

1.152

0.1

0

0.2

0.4

0.6

0.8

1

1.2

Mean

BT AT

Effect on Muscle Cramps

BTAT


Results

9

9. Effect on Atisweda

Mean


0.833 0.4 0.433

0.833

0.4

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

Mean

BT AT

Effect on Atisweda

BTAT


Results

10

10. Effect on Stoulya

Mean


3 2 1


Results

11

11. Effect on Tanohmadhuryata(FBS)

MeanDifference in

Means

S.D S.E Variance

BT AT

156.6 123.932.7 1.02 1.08 78.74


Results

12

12. Effect on PLBS

MeanDifference in

MeansS.D. S.E. Variance

BT AT

237.42 181.156.32 3.04 0.48 288

237.42

181.1

0

50

100

150

200

250

Mean

BT AT

Effect on PLBS

BTAT


Results

13

13. Effect on Mutramadhuryata

Mean


0.875 0.288 0.587

0.875

0.288

00.10.20.30.40.50.60.70.8

0.9

Mean

BT AT

Effect on Mutramadhuryata

BTAT


Results

14

Criteria for assessment of results:-

Taking into consideration of percentage of relief in clinical symptoms and clinicalparameters after the treatment.The total effect of therapy was assessed as follows.

Result Criteria for assessment

Cured 75% to 100% relief in signs and symptoms

of prameha, was taken as cured.

Moderate relief More than 50% to Less than 75% relief in

signs and symptoms were taken as moderate

relief

Mild relief Patients with improvement in b/w 25 to 50%,

in signs and symptoms were considered as

mild relief

No relief No change or less than 25% improvement in

signs and symptoms were considered as no

relief.


Results

15

RESULTS

The basis for the assessment of results was the response shown by the patients regarding

in the signs and symptoms of Madhumeha along with improvement of laboratory

investigations. The overall effect of therapy is as follows.

Result Number of Patients percentage

Cured 18 45%

Moderate relief 14 35%

Mild relief 6 15%

No relief 2 5%

Cured result was observed in 18 patients i.e 45% where patients got relief from 75% to 100%

of symptoms after the treatment. Moderate relief was in 14 patients i.e 35%, where patients

got relief from 50% to less than 75% of relief from 25% to less than 15% and mild relief was

seen in only 6 patients of all 2 patients i.e 5% where patients got relief less than 25% of

symptoms after completion of treatment.


Discussion

1

DISCUSSION

Madhumeha is a widely evidential disease since ancient age till today and evidence is

increasing day by day with lips and bounce with their complications and complexes. Diabetes

mellitus is similar to Madhumeha which is subtype of Vataja Prameha.

Madhumeha is a disease in which the patient voids excessive quantity of urine having

concordance with Madhu i.e., of Kashaya and Madhura taste, Ruksha texture and honey like

color. In Madhumeha, mainly the Vata and Kapha are predominant though the disease is

Tridoshakopanimittaja. The Vata may be provoked either directly by its etiological factors or

by the Avarana of its path by Kapha, Pitta or other Dushyas. So, Vagbhata has classified the

Madhumeha into two categories i.e., Dhatuapakarshanajanya Madhumeha and Avarnajaya

Madhumeha. Avaranajanya pathogenesis occurs due to etiological factors mainly concordant

with Kapha and Pitta, but the vitiation of Vata occurs due to Avarana.

Dhatuapakarshanajanya pathology occurs due to depletion of Dhatus, because of the Vata

vitiating etiological factors. Acharya Charaka has classified Madhumeha into

Santarpanajanya and Apatarpanajanya. The Apatarpanajanya Madhumeha can be correlated

with Dhatuapakarshanajanya Madhumeha, while the Santarpanajanya Madhumeha correlates

with Avarnajanya Madhuemeha. Therefore, this disease may be caused both by the under

nutrition as well as by over nutrition. The first type of madhumeha is considered to be

Asadhya and no specific remedy is recommended for this. But the later type has been told as

Krichhra Sadhya and can be cured with extensive measurements.

The main pathophysiology behind Diabetes mellitus is the disturbed metabolism of

the carbohydrates, fats and proteins due to either absolute or relative lack of Insulin. The

Diabetes mellitus has been broadly classified as type 1 and type 2. The type 1 Diabetes

mellitus patients are usually asthenic in body constitution and suffer from it in the early years

of life, while the type 2 Diabetes mellitus patients are usually obese and suffer from it in their

40’s. The type 2 Diabetes mellitus patients can be managed easily by hypoglycemic drugs

whereas in type 1 Diabetes mellitus patients besides hypoglycemic drugs, the Insulin therapy

is obscure. So the type 1 diabetes mellitus is nearer to Dhatuapakarshanajanya Madhumeha

while the type 2 Diabetes mellitus resembles to Avaranajanya Madhumeha.

Prameha such a disease caused predominance by vatadosha though all the 3 doshas

also take part besides ten dooshyas i.e., Rasa, Rakta, Mamsa, Medo, Majja, sukra,

ojus, Lasika, Vasa, Kleda in resulting the disease.


Discussion

2

While deciding the inclusion criteria, the terms stula and krisha Madhumeha have

been used in a much broader sense than to mean only abnormal states conveyed by

them. Krusha covers the patient who were normal to under weight. The word stula

covers the patients from normal to obese.

Somarajyadi churnam is anubhoota yoga. This preparation contains 4 drugs. They are

Bakuchi, Madhunashini, Avarthaki, Sunti. These drugs possess hypoglycemic,

neuroprotective, Medogna, Mootra Sangrahaneeyae, Rasayana, Deepana and pachana

properties.

Patients who attended O.P and I.P sections of Dr. BRKR, Govt Ayurvedic hospital

Hyd were selected randomly, irrespective of the sexes, fulfilling all the criteria for

inclusion and exclusion.

The range of Fasting and post prandial blood sugar was fixed between 120mg/dl –

180mg/dl and 160mg/dl to 300mg/dl respectively considering the safe limits of the

disease. This was done to avoid putting the patients into the risk of developing

complications as in the case of higher sugar levels.

Pre and post test design was planned and the patients were asked to take 6gms of

somarajyadi churnam half an hour before food twice daily. All the drugs are dried and

fine powedered.

The pratyatma lakshana of Madhumeha including Tanumadhuryata and

mutramadhuryata along with other common symptoms were taken for assessment.

This included the WHO approved American Diabetic association diagnostic criteria.

The symptoms were graded and scored.

Maximum number of patients belonged to the age group of 51-60 years Which

supports the views that the prevalence of type 2 DM is more in the middle to old age.

Males are more in the clinical study compared to females. Hindus were 77% which

indicative of demographic situation of this region. More number of patients was from

middle to upper middle class. This finding reflects the pattern of patients coming to

the hospital of this institute according to their socioeconomic conditions. The

incidence was also more in people who were involved in professions Who did not

involve much physical work like businessmen, shop owners and so on.

Observation of addition in the present study revealed that maximum number of

patients i.e., 40% were addicted to smoking, 10% patients were addicted to alcohol,


Discussion

3

tobacco chewing 12.5%, tea / Coffee 38.5%. All of these conditions decreased the

natural immunity and also provoke the vata to manifest the disease prameha earlier

and with severity majority of the patients i.e., 55% were suffering from the disease for

1-10 years. 45% of the patients confirmed the family history of Madhumeha which

reflects the fact that a familial trait is associated with the disease. Majority of the

patients are vatakaphaprakruti. Majority of the patients were of Madhyama to avarsara

which indicates the involvement of dhatus in Madhumeha.

On treatment with Somarajyadi churnam, the following results were observed on the

subjective symptoms.

1. Effect on Prabhootamootrata: Mild to severe prabhoota mootrata (both in terms of

quantity and frequency) was seen in 80% of patients, 65% relief was observed in

prabhutamutrata. This relief in prabhutamootrata may be due to the mutrasangrahani

action of Avarthaki and kashaya Rasa Rookshguna of Madhunashini, avarthaki which

exerts stambhana action. It may be possible that drug has acted upon apanavayu and

corrected its vitiation.

2. Effect on Avilamootrata: Only in 15% of patients avilamootrata is noted, relief was

10%.

3. Effect on Trushna: Mild to severe Trushna was seen in 70% of patients and mild to

maximum improvement was seen in 50% of patients. The relief in trushna may be

because of kaphapitta samaka effect of Avarthaki, Bakuchi and stambhana action of

avarthaki and also due to Trishnanigrahana action of sunti.

4. Effect on Stoulya: 25% patients were obese 40% of patients were over weight for

their age and height. The rest has normal weight. 25% of weight reduction is seen.

This is due to tiktarasa, kashaya rasa katu vipaka and laghu, rooksha guna and they

are having opposite qualities to that of kapha and medas . Almost 60% of the patients

had an adipose abdomen, which corroborates the fact that Indians have inherited

condition called central obesity (i.e., for a given body mass index, Indians have a

higher amount of fact than other races). There have been strong evidences implicating

this condition for the development of DM. .

5. Effect on Sweda adhikhya: Atisweda was seen in 30% of patients and 25% of

improvement was observed .vitiation of pittadosha causes swedaatipravritti. This


Discussion

4

action may be due to kashaya Rasa and stambana of avarthaki Madhunashini might

have checked the excessive sweating.

6. Effect on Dourbalya: Mild to severe Dourbalya was seen on 83% of patients,

improvement was seen in 60% of patients. Rasayana and anti oxidant properties of

Bakuchi, prevent dhatu depletion. The pramehagna properties of the ingriedients of

somarajyadi Churnam may facilitate the entry of glucose inside the cell for utilization,

thus providing energy to the cells and the patient gets relief in Dourbalya.

7. Effect on Karapadadaha: Mild to serve Karapadadaha was seen in 62% of the le

patients and mild to moderate improvement was seen in 50% of the patients relief in

Karapadadaha may be due to Kaphapitta samaka action of avarthaki, Bakuchi and

seetaveerya action of Avarthaki.

8. Effect on Karapadasuptata: 50% of the patients has mild to severe. Karapadasuptata

and mild to maximum improvement was seen in 80% of them. This may be due to

antidiabetic action of Bakuchi, Avarthaki, Madhunashini provided the relief in

Karapadasuptata.

9. Effect on Bahvashi: Mild to moderate Bahvashita was seen in 75% of the patients

16% improvement was observed. This is due to Kaphapitta samaka action of Bakuchi,

Avarthaki. This may be the reason for the relief in atikshudha.

10. Effect on Muscle cramps:Mild to moderate muscle cramps was seen in 85%

of the patients 35% improvement was observed. This is due to vatahara action of

Bakuchi and sunti.

The following were the changes observed the objective symptoms after treatment:

1. Effect on Fasting blood Sugar(FBS): The mean FBS score before treatment was

146.6 and after treatment 123.9

2. Effect on post prandial blood sugar(PPBS): The mean difference between before

and after treatment is 56.6.

Effect on FBS and PPBS may be due to the pramehagna action of Bakuchi, Avarthaki,

Madhunashi by which FBS and PPBS have reduced.

3. Effect on Urinesugar: The mean difference in the before treatment and after

treatment was 0.58%. This relief obtained could be due to the Mehagna property of

the Ingriedients of samarajyadi churnam.


Discussion

5

It was observed that the symptoms that were mild returned back to normal after 2

months of treatment but those that were moderate came down to mild and severe

symptoms reduced to moderate intensity. Moreover, the severity and number of

symptoms seemed to be directly proportional to the increase in serum glucose levels

at the upper limit of the range Usually presented with moderate to severe symptoms

than those at the lower limit of the range. Even the number of symptoms varied in that

manner.

The most of the drugs of Somarajyadi churnam have Tikata, Kashaya Rassa, Laghu,

Rookshaguna and Katuvipaka. These are said to be Kaphagna, Mehagna, Medogna and

Mootrasangrahaneeya.

Tikta, Kashayarasa, Laghu, rookshaguna produces rookshana effect and they are

having opposite qualities to that of kapha and medas. Both medas and kapha being the main

entity of Samprapti, thus by breaking the samprapti treats the disease. Hence they act as

mehagna and kaphagna.

Bahudravatva will be present in Madhumeha. Tikta, Kashayarasa present in this yoga

produces shoshana effect. Bahudravata will be reduced by the absorption of excessive fluid

from the cells. When bahudravatra of Madhumeha also reduces. Pipasa which is dependent

on Prabhutamootrata also reduces. Somarajyadi churna reduces medas there by stoulya and as

it mutrasangrahaneeya, absorbs bahudrava and hence reduces polyuria, polydipsia and

thereby checks the pathogenesis of prameha.


CONCLUSION

1. Madhumeha mostly affects the individuals after the age of forty years.

2. Sex, Marital status, Religion, Social status bear no relation in causation of

Madhumeha.

3. Tendency towards Sedentary lifestyle, increased stress and strain are main

contributing factors in the establishment of the disease. Tendency towards

sedentary life style and faulty dietary habits, leads to vitiation of kapha and meda

leadin g to Madhumeha.

4. Kapha is the arambhaka dosha and vata is preraka.

5. Etiological factors here mainly related with kapha pitta and meda vitiation but due

to avarana vata also get vitiated.

6. Apathya nimittaja nidanas influence more to cause Madudmeha in stoulya.

7. The study confirms the dominancy of kapha dosha,meda medodhatu

dusti,Rasavaha and Medovaha srotodusti in the pathogenesis of Madhumeha.

8. Madhumeha is a disease characterized by prabhoota avila mootrata, Tanu

madhuryata and Mootra madhuryata.

9. The Madhumeha has been discussed in Prameha roga as a kind of vatika Prameha.

10. It can be concluded that on the basis of symptomatology of Madhumeha, the

disease Madhumeha can be correlated with Diabetes mellitus.

11. Dhatu apakarshana and Ojo dushti is an invariable manifestation of the disease.

12. On the basis of result of the therapy it can be deduced that Asanadi qwatha

provided relief in the chief complaints, associated signs and symptoms & was

effective in reducing the blood sugar level. The mean difference in FBS was 32.7

and PPBS 56.32

13. The present study was carried on small sample for a limited time with out

alteration in their routine dietary and physical and it showed encountering results.

However to be more confirmative further study should be conducted on large

sample for longer duration with diet and exercise.


Summary

1

SUMMARY

The frame of the dissertation work entitled “A clinical study of the effect of

somarajyadi churnam on Prameha” may be summerised as follows:

The entire thesis is mainly divided into six parts each part comprises different chapter

as follows:

Part – I: Introduction, Historical background of the Disease.

Part - II: Shareeram.

Part – III:

Ayurvedic disease review was explained under subheads Nidana, Purvarupa, rupa, samprapti,

vyavacchedaka nidana, Saadhyasaadhyata, upadravas, chikitsa yojana and pathyapathya,

Modern disease reviews was explained regarding in definition, classification, pathogenesis,

prediabetic state, signs and symptoms, treatment and lifestyle management of diabetes

mellitus.

Part- IV:

The drug and its selection.

Part-V;

Method and material, observation and result.

Part VI;

Discussion, conclusion, summary, bibliography and casesheet were included.

INTRODUCTION :

The history of Madhumeha with special references to Vedas and Ayurveda are explained.

SAREERAM :

The Anatomy of pancreas and the importance of agni in Madhumeha were explained.

The mode of action of insulin in Diabetes is explained.

NIDANA:

Nidana has been classified and the types have been explained.

The basic etiology involved in the disease, has been summed-up.


Summary

2

POORVA ROOPA:

A table has been given presenting the poorvaroopas of the disease given in the classics of

Ayurveda.

ROOPA:

A generalized lakshna of disease has been stated according to different Ayurvedic classics.

The lakshnas of sahaja and apathyanimittaja prameha have been discussed in detail according

to Susrutha.

SAMPRAPTI:

The role of nidana, doshas, dushyas in the process of samprapti were explained in detail.

The samprapti in general with reference to kriyakalas have been stated.

CLASSIFICATION:

The division of 20 varietes of pramehas have been discussed in detail according to

Ayurvedic classics.

The classification of Madhumeha according to Susrutha, Vagbhata have been referred.

UPADRAVAS AND ARISTA LAKSHNAS:

The upadravas in general and prameha pidakas in particular have been classified and the

types have been discussed.

Aristalakshnas and prognosis have been explained.

SADHYAASADHYATA & SAPEKSHA NIDANA:

General information for the sadyaasadhyata of disease have been discussed in detail with

special reference to Madhumeha.

Differential diagnosis of Madhumeha has been stated in detail.

CHIKITSA & PATHYAAPATHTA KRAMA:

There is a scope for the treatment by samsodhana and samsamana for the disease has been

explained.

Tha factors of pathya and apathya are discussed in detail according to Ayurvedic classics.

THE DRUG AND ITS SELECTION:

The Drug has been described.

The criteria for the selection of the drug for the present study has been stated.


Summary

3

CLINICAL STUDY:

Method and material:-The method of preparation of medicine and the method of treatment

have been explained.

The number and nature of cases taken up for the study has been stated.

The method of observation has been explained and criteria for the assessment have been

stated.

Age and sex incidence etc. were tabulated and discussed.

The blood and urine sugar levels were recorded and tabulated. Mean, SD, SE, CHI-SQARE

test calculated.

The results of each clinical trial is tabulated.

The conclusions were drawn and are recorded.

DISCUSSION:

Total study on the disease, the drug and clinical work has been reviewed in a brief discussion.

The efficacy of the drug as observed in the clinical study has been stated and conclusions

given.


1

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3

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4

55.History of Diabetes mellitus

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59.Nidana chikitsa hastamalika - Ranajit Roy desai.

60.Kayachikitsa - Ramaraksha pathak

61.Vaidhyaka sabdasindu – Kaviraja Nagendranath sen

62.Amarakosha - Parameshwara

63.Kaiyyadeva nighantu - Kaiyyadeva krita

64.Nigantu Adarsha - Vaidhya Bapalal

65.Sabdakalpadruma - Raja Radhakantadeva

66.Sabdastomamahodadhi-Tarachandra Bhattacharya

67.Dravyaguna vignana - Yadavjitrikamji acharya

68.Review of medical pathology - Ganong


MASTER CHART

S.No Name Age Sex 1 2 3 4 5 6 7 8 9 10 Total Relieved ResultBT + + + + + + + 7 86% Cured1 Ravinder Rao 54 M AT + 1BT + + + + + + + 7 72% Mod. relief2 Kahajamiye 50 M AT + + 2BT + + + + + 5 100% Cured3 Venkata Reddy 39 M AT - - - - - 0BT + + + + + + + 7 57% Mod. Relief4 Subba Laxmi 59 F AT + + + 3BT + + + + + 5 40% Mild.relief5 Narasimha Rao 49 M AT + + + 3BT + + + + 4 75% Mod. Relief6 Narsimhulu 56 M AT + 1BT + + + + + + + 7 86% Cured7 Kasturi 62 F AT + 1BT + + + + + 5 80% Cured8 Ranga 54 M AT + 1BT + + + + + 5 60% Mod. Relief9 Rajya Laxmi 56 F AT + + 2BT + + + + 4 75% Mod. Relief10 Ramanjulu 69 M AT + 1BT + + + + 4 75% Mod. Relief11 Ravi 55 M AT + 1BT + + + + + + 6 67% Mod. Relief12 Sathya 46 M AT + + 2BT + + + + 4 80% Cured13 Laxmi Reddy 48 M AT + 2BT + + + + + + 6 50% Mild.relief14 Ramaswamy 52 M AT + + + 3BT + + + + 4 50% Mild.relief15 Sri laxmi 47 F AT + + 2BT + + + + 4 50% Mild.relief16 Kupppuswamy 55 M AT + + 2


S.No Name Age Sex 1 2 3 4 5 6 7 8 9 10 Total Relieved ResultBT + + + + + 5 60% Mod.Reilef17 Jayalaxmi 60 F AT + + 2BT + + + + 4 50% Mild.Relief18 Somaiah 57 M AT - + - + 2BT + + + + + + 5 80% Cured19 Sitamahalaxmi 49 F AT + 1BT + + + + 4 100% Cured20 Radamma 71 F AT - - - - 0BT + + + + 4 75% Mod. Relief21 Prabhakar Rao 65 M AT + 1BT + + + + 4 75% Mod. Relief22 Bhikshapathy 46 M AT + 1BT + + + + + 5 80% Cured23 Narasimhulu 51 M AT + 1BT + + + + 4 50% Mod. Relief24 Jyothiprakash 40 M AT + + 2BT + + + + + 5 100% Cured25 AVRJ Raju 42 M AT - - - - - 0BT + + + + + 5 80% Cured26 Suresh 49 M AT + 1BT + + + + + 5 60% Mod. Relief27 Maqbool 58 M AT + + 2BT + + + 3 67% Mod. Relief28 Jagadeswari 46 F AT + 2BT + + + + + 5 80% Cured29 Sriramurthy 60 M AT + 1BT - - - + - - - + + + 4 25% No Relief30 Sreebabu Rao 60 M AT - - - + - - - + - + 3BT + + + + 4 75% Mod.Relief31 Subramanyam 63 M AT + 1BT + + + + + 5 0 No relief32 Kanaka Durga 47 F AT + + + + + 5BT + + + + + 5 80% Cured33 Nagaraj 52 M AT + 1


S.No Name Age Sex 1 2 3 4 5 6 7 8 9 10 Total Relieved ResultBT + + + + + 5 100% Cured34 Sandhya 60 F AT - - - - - 0BT + + + + + + + 7 72% Mod. Relief35 Nilina 45 F AT + + 2BT + + + + 4 25% Mild relief36 Prabhakar 50 M AT - + + + 3BT + + + + + 5 80% Cured37 Ramasastry 62 M AT + - - - 1BT + + + + 4 25% Mild38 Vinod 40 M AT - + + + 3BT + + + + + 5 80% Cured39 Raja 46 M AT + 1BT + + + + 4 100% Cured40 Swapna 40 F AT - - - - 0

1) Prabootamutrata 2) Avilamutrata 3) Atitishna 4) Atikshuudha 5) Suptata 6) Dourbulya 7) Karapadadana 8) Musclecramps9) Stoulya 10) Atisweda


A Clinical Study of the Effect of Somarajyadi

Churnam In the Management of Prameha.

By

Dr. KAVITHA REDDY B.A.M.S

Under the Guidence of

Dr.V.VIJAYA BABU M.D.(Ay)

Reader/Professor K.C

Post Graduate Dept of Kayachikitsa

Dr. B.R.K.R. Govt. Ayurvedic College, Hyd.


Charaka in his Charaka samhita has mentioned thesweetness of urine in addition to polturia.

Susrutha in 500 A.D described the disease asMadhumeha with symptoms of foul breath,voracious appetite and languor.

Generally Madhumeha is known as a “richmansdisease”

Prameha is a chronic disease of relapsing nature. Thedisease is also a debilitating one.


HISTORY

Charaka explained the etiology, pathogeness, symptomatology,complications and treatment modalites in detail in Nidana 4th and chikitsa6th chapter. While in sutra sthana 17th chapter he described theavaranajanya pathogenesis of Madhumeha, this is the unique contributionof this treatise.

Susruta also explained Prameha in elaborative manner with separatechapter on its management. He used ‘Kshoudrameha’ synonym toMadhumeha in nidana 6th chapter.

Harita mentioned it as papajanya and enumerated 13 types of prameha.

Bhela described prameha is of two types.

Kashyapa mentioned the symptoms of prameha child in vedanadhyana andnoted the disease as chirakari.


SHAREEMThe pancreas is a compound alveolargland. It has got

both exocrine & endocrine function. Diabets mellitus is achronic disease due to disordered carbohydrate metabolismand it results due to deficiency of insulin secreted by theBeta cells of islets of Langerhans of pancreas.

The exocrine portion of pancreas consists of acinigrouped into lobules. The exocrine pancreas made up ofisolated group of cells the islets of langerhans.

Endocrine portion (Islets of langerhans)It is an endocrine organ which exert a profound

effect on carbohydrate metabolism.


In endocrine portion 4 cells are present(1) cells (2) cells (3) cells (4) F cells

cells synthesise and secrete glucogon and cellsproduce insulin and D cells have been linked with eithergastrin or secretin production. F cells secretes pancreaticpolypeptide (PP)

The islet volume comprises 1-1.5% of the total massof the pancreas and weighs about 1-2g in adult humans.

The first harmone to be identified as a product of theislet was insulin.


Mechanism of Insulin Secretion

Increased Sugar Level

Translation GLUT

Uptake of Glucose by cells

Release of Insulin

If Stimulation Persists

Active Synthesis of Insulin


Biological Effects of Insulin

A) On Carbohydrate Metabolism:-Reduces the rate of release of glucose from liver.

By inhibiting glycogenolysis By stimulating glycogen synthesis By stimulating Glycolysis By indirectly inhibiting gluconeogenesis via inhibition of fatty acid

mobilisation from adipose tissue.B) On Lipid Metabolism:- Reduces the rate of release of free fatty acids from adipose tissue. Stimulates fatty acids synthesis and also conversion of fatty acids to

triglycerides in liver.C) On Protein Metabolism:- Stimulates transport of free amino acids across the plasma Membrane in

liver and muscle. Stimulates protein bio synthesis and reduces release of amino acid from

muscle


NIDANANidana for premeha of each dosha were mentioned in Charaka Nidana 4th

Chapter.

Ch, A.S., A.H.Ekasthanasanarati, SayyasanaswapnaSukham

12

A.S., A.H.Sura11

Ch, A.H., A.S., SuAnnapana having Snigdna, guru, picchila,Seeta, drava, Medokara gunas

10

Su, A.H., A.S.Madhura rasa, Amlarasa, Lavanarasa –Ahara having these Rassas

9

Su, A.S., A.H.All the Ahara Vihara factors which vitiatemedas, Kapha, mutra

8

Ch, A.S., A.H., B.PGudavikaras & Guda7

Ch, A.S., A.H. B.P.Navannapanam, Navadravyas, Navadhanya6

CharakaKsheeram5

Cha, A.H., A.S.Gramya, anupa, oudaka – Mamsa RasaSevana

4

Ch, B.PDadhi3

ChSwapnasukham2

ChAsyasukham1

ReferenceNidanaS.No 9


Poorva Rupa

Ch. NiShatpadapipeelikabiccha shareera Mutrabhisaranam13.

Ch.Ni.ch.Chi, A.S.NiMutrebhidravanti pipeelikanam Mutrechnamutradosham12.

Ch.Ni., A.S.NiAngeshusuptata11.

Ch.Ni. A.S.NiParidaham10.

Ch.NiKayachidreshupadeham9.

Ch.Ni, A.S.NiKayemalam8.

Chi. NiThrut7.

Su.Ni, A.S.Ni. A.H.NiPipasa6.

Ch.Ni, Ch.Chi. Su.Ni, A.S.NiMukhatalukanta sosha, talugala sosha5.

Chi.Ni,Cha.chi, Su.Ni, A.H.NiKarapadadaha4.

Ch. NiKarapada suptata3.

Ch.Ni,Ch.Chi, A.S.ni, A.H., NiAsyamadhuryam2.

Ch.Ni, Su.Ni, A.S.NiJatileebhavam Kesheshu1.

ReferencePoorva RupaS.No

Poorva Rupa


ROOPARoopa of a disease will be produced in the fifth stage of samprapti i.e., Vyaktavasta.

Samanyalakshanas:-

1) Prabhootamootrata:- Vagbhata mentioned prameha as the disease ofmutratipravritaja vikara. Patient voids urine more in quantity and frequency.Gayadas opines that this excess urine quantity is because of liquification ofthe dushyas and their amalgamation.

2) Avilamootrata: Patient voids urine having turbidity.

Sarvadaihika Laxana:-Sahaja Apathyanimihaja

1) Krisha(Emaciated) 1) Stulatwa (obese)2) Ruksha (dryness of body) 2) Snigdha (Unctous)3) Alpasi (poor eatingdesire) 3) Bahwasi (polyphagia)4) Pipasabhrusam(intense thirst) 4) Shayya Asana Sukham (desirous for

posture and lying down on bed)5) Parisaranasheela (Tendency of 5) Swapnashila (constant tendency for

roming) sleeping)


CLASSIFICATION

UdakamehaIkshumehaSikatamehaSanairmehaSandramehaSukramehaPistamehaSeetamehaAlalameha

UdakamehaIkshumehaSikatamehaSanairmehaSandramehaSukramehaPistameha(su.ni6/8)Surameha(su.ni6/8)LavanamehaPhenameha

1) udakameha2) Ikshumeha3) Sikatameha4) Sanairmeha5) Sandrameha6) Sukrameha7) Shukla meha8) Sandraprasada9) Seetameha10) Alalameha

Kaphaja 10types

VagwnataSusrutaCharakaDosha

VasamehaMajjamehaHastimehaMadhumeha

VasamehaHastimehaKshoudrameha(su.ni6/8)Sarpirmeha

1) Vasameha2) Majjameha3) Hastimeha4) Madhumeha

Vataja 4 types

KsharamehaKalamehaNeelamehaRaktamehaManjistamehaHaridrameha

KsharamehaNeelamehaSonitamehaManjistamehaHaridramehaAmlameha(su.ni6/8)

1) Ksharameha2) Kalameha3) Neelameha4) Lohitameha(ch.ni4/24)5) Manjistameha6) Haridrameha

Pittaja 6 types


SAMPRAPTISamprapti is a process by which dosha dushyasamsarga will takes

place and finally manifests the disease.• Sampraptighataka of madhumeha:• Dosha : Sleshma pradhana tridosha sleshma is the main dosha

responsible for Madhumeha inspite of the fact that madhumeha is atridoshajanyavyadhi. The other doshas like vata& pitta only trigger offthis samprapti and associate as anubandha.

• Dushya : Rasa, Rakta, Mamsa, Meda, Majja, Sukra Vasa, lasika,ojus, kleda

• Srotodusti : The srotodusti laxana occur as sanga of kapha leading tovimargagamana and atipravritti of kleda through the mootra.

• Agni : Vaishamya of all agnis (or dhatvagnimandya)• Ama : Medogata ama produced due to jataragni mandhya and

dhatvagnimadhya.• Adhistana : vasti• Udbhavasthana : Amasaya• Bhedavastha : Occurance of upadravas such as puti mamsa,pidaka

etc.• Nature : chirakari, anusangi


CHIKITSAChikitsa sutra:-

Stulapramehi balavanihaika krisastadaika paridurbalascha.

Sam Brimhanam Tatra Krisasya karyam Samsodhanam Doshabaladhikasya.(Cha.Chi

6/1)

• Charaka classified patients of prameha into two categories for treatment

purpose.(cha.chi. 6/15 – 17& 18)

• Stula – Samsodhana therapy was prescribed.

• Krisha – Brumhana & Samsamana therapy was prescribed.

• The samsodhana kriya vamana, langhana adopted at appropriate times to cure

kaphaprameha.

• The virechana kriya, Santarpana kriya, samanakriya cure pittajameha

(cha.chi.6/23)

• A krisha or emaciated patient who is not capable of with standing the

purificatory procedures requires Brimhana kriya(cha.chi 6/15)


Bakuchi

DRUGS

Madhunashini

AvarthakiNagara


SOMARAJYADI CHURNAM


DRUG REVIEWDrug plays a vital role in the management of the disease.Due to this reason, it had been

placed next to physician in the chatuspada.• The best drug is that which cures the disease promptly and also preserves or sustains

the helath of an individual.• The drug selected for present clinical study on prameha is “SOMARAJYADI

CHURNAM”.SOMARAJYADI CHURNAM:-• Somrajyadi churnam is anubhutayoga to prove its scientific efficacy.Ingredients:-1. BAKUCHI,(Psoralea corylifolea) - 1 part2. AVARTHAKI,(Cassia auriculata) - 1part3. MADHUNASHINI, (Gymnema sylvestris) - 1 part4. SUNTI(Zingiber officinale) - 1partAll are taken in equal parts and fine powdered.DOSE:-6 grams/ dayANUPANA:-Sukoshna jalam

Most of the drug have tikta, kashayarasa,laghu , rooksha guna, katuvipaka.These aresaid to be kaphagna, mehagna, medogna.

Tikta, kashayarasa, laghu, rookshaguna produces rookshana effect and they are havingopposite qualities to that kapha and medas.

Bahudravatva is present in madhumeha. Tikta, kashayarasa produces shoshana effectand there by bahudravatva is reduced.


Materials and methodsMy dissertation entitled “A CLINICAL STUDY ON THE EFFECT OF SOMARAJYADI

CHURNAM IN THE MANAGEMENT OF PRAMEHA “ was carried out on 40 patientswho attended the OP and IP sections of Govt.Ayurvedic college/Hospital, Erragadda.HYD.during Jan 2007 to sep2007.

Aim of study:-1.To evaluate the effect of “SOMARAJYADI CHURNAM”in patients suffering from stula and

krisha Madhumeha.2.To evaluate the effect of Somarajyadi churnam in NIDDM patients.3.Comprehensive literary study on prameha.– 1.Materials:-– patients– drugs– Patients :- 40 patients were taken for the study.– Drugs:- Somarajyadi churnam with sukoshna jalam– 2. Methods:-– 1.Location of study:- For the purpose of clinical trials 40 patients were selected from OP and

IP department of Kayachikitsa of Dr.B.R.K.R Govt.Ayurvedic college/hospital,Erragadda,Hyderabad.

– 2.Selection of patients:- 40 patients of different age groups were selected on the basis ofFBS&PLBSand corresponding urine sugars.

– Diagnostic criteria:-– Criteria - 1:- patients presenting with pratyatma lakshana of Madhumeha –prabhoota and

avilamootrata with mootra or tanumadhuryata with or without roopa are taken as Madhumehi.– Criteria -2:-– FBS -80 -120mg/dl– PLBS -140 -180mg/dl


– Inclusion criteria:- patients fulfilling the following conditions wereincluded.

– patients between 30yrs -70yrs.– Stula and krisha Madhumehi.– Patients with Type 2DM with FBS greater than 120mg/dl and lesser than

180mg/dl and PLBS of more than 160mg/dl and less than 300mg/dl.– Exclusion criteria:- The following patients were excluded from the

study.– 1.patients below 30yrs.– 2.Jatapramehi– 3.IDDM patients– 4.Gestational diabetes– 5.DM secondary to drugs like corticosteroids or due to secondary

disorders– Investigations:-– 1.FBS– 2. PLBS– 3.Urine sugar– Research design:-– A single blind clinical trail with pre and post test design was adopted.– Intervention:-– Intervention was done with Somarajyadi churnam taken,the 4 drugs in

equal parts and the powder is given in 2 divided doses.i.e 6 grams in 2doses with sukhoshnajalam before food.


Observation1.Age Incidence 2.Sex incidence

31-40

41-50

51-60

61-70

M a le

Fe m a le

6

34

0

5

10

15

20

25

30

35

Single Married

Marital Status

Series1

3.Marital Status 4. Religion Incidence

Hindu

Muslim

Christian


5. Socioeconomic status

0

56

15

10

4

0

2

4

6

8

10

12

14

16

UP P LM M UM R

Socioeconomic status

Series1

6. Incidence of Addictions

16

54

15

0

2

4

6

8

10

12

14

16

Smoking Tobacco Alcohol T/C

INCIDENCE OF ADDICTIONS

Series1

7. Socioeconomic status 8. Deha prakriti

Veg

Mixed 6

3

14

9

3

5

0

2

4

6

8

10

12

14

VP PV VK KV PK KP

DEHA PRAKRITI

Series1


9. Satva Incidence

Pravara

Madhyama

Avara

14

0

15

11

0

2

4

6

8

10

12

14

16

Teekshna Sama Vishama Manda

STATUS OF AGNI

Series1

8

26

6

0

5

10

15

20

25

30

Pravara Madhyama Avara

BALA INCIDENCE

Series1

FirstDegree

Seconddegree

Nofamilialhistory

10.Status of Agni

11. Bala Incidence 12.Family History


EFFECT OF THE TREATMENT:-

41164802025Karapadadaha9

1711716646Avilamutrata2

234112661218Suptata7

36629535617Musclecramps10

18693732433Dourbalya8

133133741622Tanohmadhuryata

6

165238612134Mutramadharyata

5

247247541630Atikshudha4

236103671928Atitrishna3

62134812632Prabhootamutrata

1

%Unchanged%Improved%Reliver

d

No.of CasesTotalNo. ofCases

Signs & SymptomsS.NO


RESULTS

1.875

1.538

0

0.5

1

1.5

2

Mean

BT AT

Effect on Prabhoota Mutruta

BT

AT

1.5

1.25

1.1

1.15

1.2

1.25

1.3

1.35

1.4

1.45

1.5

Mean

BT AT

Effect on Avilamutrata

BT

AT

0.3371.5381.875

ATBT

Differencein Means

Mean

0.251.251.5

ATBT

Differencein Means

Mean


0.251.251.5

ATBT

Differencein Means

Mean

1.286

1.158

1.081.1

1.121.141.161.181.2

1.221.241.261.281.3

Mean

BT AT

Effect on Atitrushna

BTAT

1.333

1.25

1.2

1.22

1.24

1.26

1.28

1.3

1.32

1.34

Mean

BT AT

Effect on Atikshudha

BTAT

0.1281.1581.286

ATBT

Differencein MeansMean

0.0831.251.333

ATBT

Differencein Means

Mean


0.2771.1671.444

ATBT

Differencein MeansMean 1.444

1.167

0

0.2

0.4

0.6

0.8

1

1.2

1.4

1.6

Mean

BT AT

Effect on Karapadasuptata

BT

AT

1.2

0.85

0

0.2

0.4

0.6

0.8

1

1.2

Mean

BT AT

Effect on Karapadadaha

BTAT

0.350.851.2

ATBT

Differencein MeansMean


123.9

156.678.74

1.081.0232.7

ATBT

Variance

S.ES.DDifference

in MeansMean

237.42

181.1

0

50

100

150

200

250

Mean

BT AT

Effect on PLBS

BTAT

181.1237.42

2880.483.0456.32

ATBT

Variance

S.ES.DDifference in

MeansMean


Criteria for assessment of resultsResult Criteria for assessmen

Cured 75% to 100% relief in signs andsymptoms

Moderate relief More than 50% to Less than 75%Mild relief Patients with improvement 25 to

50%, reliefNo relief No change or less than 25%

Results Number of Patients percentage

• Cured 18 45%• Moderate relief 14 35%• Mild relief 6 15%• No relief 2 5%


DISCUSSION• Prameha is a disease caused predominance by vatadosha though all the 3 doshas also

take part besides ten dooshyas i.e., Rasa, Rakta, Mamsa, Medo, Majja, sukra, ojus,Lasika, Vasa, Kleda in resulting the disease.

• The range of Fasting and post prandial blood sugar was fixed between 120mg/dl –180mg/dl and 160mg/dl to 300mg/dl respectively.

• The pratyatma lakshana of Madhumeha including Tanumadhuryata andmutramadhuryata along with other common symptoms were taken for assessment. Thesymptoms were graded and scored.

• Maximum number of patients belonged to the age group of 51-60 years Which supportsthe views that the prevalence of type 2 DM is more in the middle to old age. Males aremore in the clinical study compared to females.

• Maximum number of patients i.e., 40% were addicted to smoking, 10% patients wereaddicted to alcohol, tobacco chewing 12.5%, tea / Coffee 38.5%. All of these conditionsdecreased the natural immunity and also provoke the vata to manifest the diseaseprameha.

• Majority of the patients are vatakaphaprakruti. Majority of the patients were ofMadhyama to avarsara which indicates the involvement of dhatus in Prameha.

• Effect on Prabhootamootrata: Mild to severe prabhoota mootrata (both in terms ofquantity and frequency) was seen in 80% of patients, 65% relief was observed inprabhutamutrata. This relief in prabhutamootrata may be due to the mutrasangrahaniaction of Avarthaki and kashaya Rasa Rookshguna of Madhunashini, avarthaki whichexerts stambhana action. It may be possible that drug has acted upon apanavayu andcorrected its vitiation.

• Effect on Avilamootrata: Only in 15% of patients avilamootrata is noted, relief was10%.

• Effect on Trushna: mild to maximum improvement was seen in 50% of patients. Therelief in trushna may be because of kaphapitta samaka effect of Avarthaki, Bakuchi andstambhana action of avarthaki and also due to Trishnanigrahana action of sunti.


Effect on Sweda adhikhya: Atisweda was seen in 30% of patients and25% of improvement was observed .

Effect on Karapadadaha: Mild to serve Karapadadaha was seen in 62%of the le patients and mild to moderate improvement was seen in 50%of the patients.

Effect on Bahvashi: Mild to moderate Bahvashita was seen in 75% of thepatients 16% improvement was observed. This is due to Kaphapittasamaka action of Bakuchi, Avarthaki. This may be the reason for therelief in atikshudha.

Effect on Fasting blood Sugar(FBS): The mean FBS score beforetreatment was 146.6 and after treatment 123.9

Effect on post prandial blood sugar(PPBS): The mean differencebetween before and after treatment is 56.6.

Effect on Urinesugar: The mean difference in the before treatment andafter treatment was 0.58%.

The most of the drugs of Somarajyadi churnam have Tikata, KashayaRassa, Laghu, Rookshaguna and Katuvipaka. These are said to beKaphagna, Mehagna, Medogna and Mootrasangrahaneeya.

Tikta, Kashayarasa, Laghu, rookshaguna produces rookshana effect andthey are having opposite qualities to that of kapha and medas.


CONCLUSION• Prameha mostly affects the individuals after the age of forty

years.• Sex, Marital status, Religion, Social status bear no relation

in causation of Madhumeha.• Tendency towards Sedentary lifestyle, increased stress and

strain are main contributing factors in the establishment ofthe disease.

• Kapha is the arambhaka dosha and vata is preraka.• Apathya nimittaja nidanas influence more to cause

Madudmeha in stoulya.• Madhumeha is a disease characterized by prabhoota avila

mootrata, Tanu madhuryata and Mootra madhuryata.• Dhatu apakarshana and Ojo dushti is an invariable

manifestation of the disease.


Prameha kc015 hyd

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