My commitment increases my level of energy. My energy increases my level of action. Myaction increases my level of success. My success increases my level of commitment.

Research in any field is the most important section of development. Ayurveda is inservice is for ages to the needy mankind to relieve their ailments and recording the factsfor the future generations. At present the Ayurveda research scholar, developing theAyurveda and understanding under the limelight of contemporary scientific backgrounds.The plagiarism is more and more now a day in the scientific community. This ishappening as the researches of the various institutions are not available for the commonresearcher. We wish to control this plagiarism by contributing the dissertations forscientific community. If you find any thesis is a copy of the previous publication, we takethis issue to the university authorities for proper action. The solution to prevent copy catsis … http://ayurvedaresearch.wordpress.com/

Dr. Shiva Rama Prasad Kethamakka

technoayurveda@gmail.com,

ACKNOWLEDGEMENT

I express my profound gratitude to my respected and honorable guide

Dr.V.VIJAYA BABU M.D. (Ayu.), Professor, P.G. Unit of Kaya Chikitsa., For his

excellent guidance and co-operation conducting this research work successfully.

I am highly indebted to my honoroble Dr. PRAKASH CHANDRA M.D. (Ayu.),

Proffessor Head of the department of Kayachikitsa, for his valuable timely

suggestions, thought provoding leads ideas and support in Completing this thesis

work.

I am very thankful to my co-guide Dr. RAMALINGESWARA RAO garu,

Technical Assistant and Lecturer for their precious suggestions and help through out

the study.

I convey my gratitude to the honorable Principal Dr. SADASIVA RAO, and Ex-

Superintendent L. RADHA KRISHNA MURTHY and Present Superintendent V.L.N.

SASTRY of Dr. B.R.K.R. Government Ayurvedic Hospital

I am thankful to Dr. V.V.S. RAMA SASTRY, M.D.(Ayu.), Retired professor,

and Dr.VASUDEVARAO garu retired professor, Dr. BASWANT garu Retired

Professor, Dr. M.L. NAIDU garu for their valuable suggestions and encouragement.

I am also thankful to teaching staff, Post graduate department of Kaya Chikitsa

especially Dr. VIJAYA LAKSHMI garu, Dr. NAGESWARA BABU garu, for their

precious suggestions and help throughout the study.

I express highly thankful to my Parents Sri K. RAMAKRISHNAIAH & Smt.

ARUNA whose love, support and encouragement for the initiating sources, which

directed me towards progress and success in each and every step of my life.

I express my special thanks to my Family members Mr. Vijay Kumar, Mr.Guru

Murthy, Mr. Prabhakar, Mr. Sambasivam, Prasanth, Chinnamma, Bhagya

Lakshmi, Suneela, Sujatha, Seshanka, Surya Teja, AND Ganesh for the valuabe

support which made this work possible.

I thank to my good neighbours Smt. Rajamani Garu, Mr. Srinivas & Neeraja,

whose moral support has my spirit in difficult situations.

It is pleasure to convey my thanks to my Co-PG Schoolars and friends especially

Dr. Jayalakshmi and her mother, Dr. Gnana Prasuna and her mother, Dr. V.K.M.

Lavanya, Dr.Padmaja, Dr. Sireesha, Dr. Namrata, Dr. Usha Madhuri, Dr.

Nageswara Rao, Dr. Ravi, Dr.Sivarama Krishna, Dr. Gayatri, Dr. Madhavi, Dr.

Geetha, Dr. Kavitha and Dr. Sandhya for their constent support and helped me

throughout this thesis work directly and indirectly.

I special thanks to Dr. Yashoda MD (Ayu.) lecturer, in B.R.K.R. Ayurvedic

College for her valuable suggestions and encouragment.

I sincerely thankful to Smt. Mamatha & Mr. Chakravarthy, VS GRAPHICS

helps me in the computerized of the thesis.

Hyderabad

February 2008 (Dr. K. SUNEETHA)

CONTENTS

PART – I PRELIMINARY PART

1. Intorcution 1

2. Historical Review of the disease

PART - II THE DISEASE - PANDU ROGA

1. Definition & Synonyms of the Disease 7

2. Classification 9

3. Sareera (Rachana & Kriya) 13

4. Nidana 40

5. Poorva Roopa 48

6. Roopa 51

7. Samprapti 64

8. Sadhya and Asadhya Lakshanas 67

9. Upadravas and Arishta Lakshanas 69

PART - III CHIKITSA

1. Chikitsa krama 71

2. Pathyas and Apathyas 78

PART-IV DRUG REVIEW

1. Criteria for selection of Drug 80

2. Description of individual drugs 82

3. Mode of preparation 99

PART V CLINICAL STUDY

1. Materials and Methods 101

2. Observations 105

3. Results 112

PART - VI

1. Discussion 121

2. Conclusion 125

3. Summary 127

PART - VII

Special case sheet for Pandu Roga130

2. Bibliography 134

INTRODUCTION

Ayurveda is origin from vedas, mainly from Adharavana veda. According to

Ayurveda, definition of health includes both physical and mental well being and

treatment was mentioned for both Swastha in order to preserve health and Atura in

order to treat the disease.

Chaaya and prabha are associated with skin and are based on the condition of

Bhrajaka pitta. The discoloration like the colour of ketaki dooli, swetha, peeta, harita

etc., are the manifestations of pathological process caused not only by the etiological

factors of vitiated doshas but also by consumption of mrit in pandu roga.

The pandu roga is one of the commenest alitments prevalent not only in India

but also world wide. The panduroga is included under the heading of

"Varnopalakshita Roga" ie., Varna pradhanya disease. It is known since ancient

times. The disease is referred as Vilohita, Harima, and Halima in vedas and susrutha

named it as Panaki, Laghavaka and Kumbhahwa.

William D.Whitney an eminent authority of vedic literature compared viloma

with anaemia. It is the commonest disease irrespective of age, sex and religion. It is

prevalent in women, pregnant in specific. As the prevalance of the disease is more

comparatively research studies are needed to evalutate proper eradication procedure,

with the help of the system of medicine which has been existing since many centuries

i.e. Ayurveda. The iron deficiency is the commonest nutritional dificiency world over

and its prevalence is highest in India.

According to NFHS suffering with Anaemia.

Female Children

All over India 50% 70-72%

Andhra Pradesh 52% 75%

Panduroga can be compared to a state of Anaemia in modern system of

medicine, in which the haemoglobin concentration falls bellow the accepted normal

range due to the failure of haemoglobin synthesis and other conditions mentioned in

nidana and sareera. In particular where unhygienic, low socioeconomic and faulty

food habits are the contributing factors. It is even more common in pregnant women.

Its prevalence in all the age groups and in both the sexes interested reserchers right

from ages.

The Ayurvedic classics have mentioned a number of effective formulations for

treatment of pandu roga keeping in view of the above factors, the present study

entitled as "A clinical study on the effect of Bhaskara lavana choornum in pandu

roga" is carried out.

The efficasy of this formulation in pandu roga can be justified by its indication

in Alpa rakta condition explained in the pages that follow. The preparation Bhaskara

Lavana churna is taken from Agnimanandya chikitsa Adhyaya of Bhaishadjya

Ratnavali. The drug fulfils the qualities of Bahu guna, Yogya, Sukha aswadana,

Preenana, vyadhi nashana, avipathkara and gandha varna rasopeta.

Thirty patients are randomly selected from those attending the out patient

department of post graduate unit of kayachikitsa, Dr. B.R.K.R. Govt. Ayurvedic

college / Hospital, Erragadda, Hyderabad. The drug Bhaskara lavana churna is tried

on 30 patients and results are assessed periodically.

The results are encouraging, which are discussed in length, in the chapter of

results seperately, the entire work is devided into VII parts, covering all the aspects of

the disease. Pandu roga and Drug Bhaskara Lavana Churnam.Part I consists of introduction and historic review of the disease. Part II consists of

various aspects of the disease such as definitions, synonyms, classification, sareera

Rachana, Sareera kriya, Nidana, Samprapti and other aspects. Part III consists of

chikitsa krama of pandu roga in general. Part IV consists of various aspects of drugs in

detail. Part V consists of clinical study, under which, materials and methods,

observation and results are included. Part VI consists of discussion, conclusion and

summary. Part VII consists of special case sheets and Bibliography.

HISTORICAL REVIEWAyuevedia is the most ancient system of medicine among the different systems

of medicine existing.

Vedas are apourshayas. Vedas are the oldest knowledge books known to men

according to Indian thought. So, it would be appreciable to explore the history right

from the period of Vedas to present period. On the scale of time, next to Veda are

Puranas, Upanishads and Brahmanakas, Samhitas, Sangrahas, Nighantus and

Arvacheenakala Grandhas. Now, let us consider some of the points related to

Panduroga mentioned in different texts/literature/knowledge available till date in a

stepwise manner under the following headings.

1. Veda Period

2. Purana Period

3. Samhita and Samgraha Period

4. Avracheena Period

1. Vedic Period: In Vedas there are many references about the disease Pandu.

Rigveda: Pandu roga has been mentioned under the name Harima. 'Suryanamaskaras'

and prescribed as its treatment in Rigveda.

2. Yajurveda: In Yajurveda there is a reference about Pandu. A reference from this

veda quoted that there is some relation between yakrit, kloma and pitta in relation to

Panduroga. Charaka and Susruta has elaborated this point in detail by stating that the

moolasthana of raktavaha srotas lies with yakrit and pleeha and the predominant dosha

associated with Pandu is pitta.

3. Atharvanaveda: This veda reiterated the same as above. There are references like

Vilohita, Harima, Halima which can be taken as synonyms of Pandu. The significance

of sun rays is stressed in Atharvana veda for changing the colour in Pandu roga.

Another reference from Atharvanaveda advocates godugdha as a remedy for

Panduroga.

4. Pouranika kala:Garuda Purana, valmiki Ramayana and Agni purana have also

mentioned about 'Pandu roga'. In Garuda purana lohachoorna with takra anupaana is

prescribed especially for Pandu patients, and Nidana, Lakshanas, Pathyaapathya

vicharanas are also explained in detail.

Mahabharata states that the Hastinapura king had suffered from Pandu roga

whose name itself is Pandu Raju. He acquired the disease as a curse from a saint. This

explains the karmasiddhanta of Panduroga. King Pandu acquired sterility due to Pandu

Roga as a complication and he even died of the disease.

5. Samhita & Sangraha kala: This is the golden period of ayurveda, since most of

the Ayurvedic Classics like Charakasamhita, Susruthasamhita, Bhelasamhita,

Hareetasamhita, Kasyapasamhita took shape in this period. These samhitas are the

basis of Ayurveda that is being practiced throughout the world. Panduroga has been

described in detail along with treatment in all classics as stated below.

Name of the book Sthana Chapter No.

1. Charaka Samhita Chikitsa 16th

2. Susruta Samhita Uttara 44th

3. Astanga Sangraha Nidana 13th

4. Astanga Sangraha Chikitsa 18th

5. Astanga Hridaya Nidana 13th

6. Astanga Hridaya Chikitsa 16th

7. Sarangadhara samhita Poorvakhanda 7th

8. Madhavanidana 8th

9. Bhavaprakasha Madhyamakhanda 8th

10. Vaidhya chintamani Pradhama samputa 4th

Even the works such as Chakradatta, vangasena, Yogaratnakara,

Bhaishajyaratnavali, Basavarajeeyam, Madhavanidanam and Sarangadhara samhita

also give a detailed description of Pandu roga.

We can find references of a number of medicinal plants that are proved to be

useful in Panduroga in Dhanvanthari, Kayyadeva and Astanga nighantus. The author

of Vidhyachintamani Srimad Indrakanta vallabha charyulu stated that Pandu is a

senapathy (chief of army) for the disease Kshaya.

With the advent of Rasakala, some mineral and metallic preparations replaced

the herbal drugs, after shodana and marana. Rasaratnasamucchaya, Rasapadhati and

other literatures on Rasashastra have thousands of preparations which are prescribed

for the management of Pandu.

5. Aravacheena Period: This is the starting period of modern system of medicine,

William D. Whitney, who is a known authority on vedic literature compared vilohita

mentioned in Vedas to anaemia.

Hippocrates, the father of modern medicine in 460BC, described anaemia like

symptoms such as pallor and weakness. he attributed these symptoms to the chagnes

of blood. Anaemia, in those days, was found predominately in virgins and was hence

called demarbo virgina (the sickness of virgins) by Dr. Johanns Large in 1554 A.D.

He described this is pallor of checks, breathlessness on exertion, increased pulsation

of the temporal vessels and dysponea on climbing stairs or dancing. This illness was

later termed Chlorosis and clinical use of iron was first initiated in 17th century by

Thomas Sydenham.

Dr. Grambiel andral succeeded in describing the changes of blood

micorscopically in Anaemia during 1797-1876.Also the work of Thomas Addison, during the same period contributed to the

discovery of one of the type of anaemias - The Addision's Anemia. This is later on

termed as Perinicious Anemia, After the efforts of Dr. Wilks in 1855 and Dr.

Biermer's in 1872. Another type of anemia - Spleenic Anemia was described by Dr.

Banti in 1882. Dr. Minot and Dr. Murphy in 1926, conducted a trial of diet consisting

of liver and beef, which are rich in iron. this showed considerable improvement of

Perinicious Anemia. However, they could not provide enough explanation for the

same. This was bridged by the muchapplauded work of Dr. Castle.

G.R. Minot, W.P. Murphy and G.H. Whipple in 1934 shared Nobel Prize in

Physiology and Medicine for their work concerning the treatment of Anaemia with

liver. In 460BC Hippocrates also explained the importance of consumption of liver in

combating anaemia during pregnancy. The same was also recommended by Charaka

and Susrutha in 500 B.C.

Now-a-days, there are many clinical, pathological, and diagnostic technologies

available in regards to Anaemia. As per Modern system of medicine, anaemia is of

many types. It is being treated on the whole by supplement of Iron and its source in

the form of daily nutrition or in medicines which would be seen in detail in the topics

that follow, as and when in need. This disease is prevalent in most communities due to

various causes and yet a lot has to be achieved.

The above review clearly indicates that Pandu is blood related disease, its

relation is to Raktavaha srotomoolas has long back been mentioned and Ayurvedic

physicians were aware of the disease and its management since vedic period. Thus

history of Pandu and its corelated disease. The Anaemia of Modern system of

medicine has been briefly outlined.

References:

1. Mc. Odonell and Keeth Vedic Index Vol II.

2. Whintney, W.D. Translation of Atharvana Veda, by Motilala Banarasidas,

1962.

3. Garuda Purana Chapter 184/29

4. A short history of Medicine II Edition by Singer and Underwood.

5. Pandu Roga by Pathak R.R. Published by C.A.R.I., 1987

6. Henry A.S. The Origin of the medical terms, Batlimore 1961.

7. Vedomme Ayurved.

8. Susruta Samhita Uttara sthana 44th chapter.

9. History of Indian Medicine by Dr. Rama Rao, P.V. Sharma and Others.

DEFINITION AND SYNONYMS

Charaka classified rogas according to Ruja, Varna, Samuthana, Samsthana

and Stana. In this classification the disease pandu falls in the group of varna. In panduroga there is some significant change in the normal colour of the body.

There are many definitions in Ayurvedic literature. One nirukti quated by vijaya

rakshit is

“Pandutwenopo lakshito roga pandu roga”

(madukosa)Which difenes that a person who acquires pandu varnatvam is a pandu roga.

“Swetha peeta samayukta panduvarna prakirtitaha”(Amarakosa)

The combination of white and yellow colours in equal proportion are called

pandu roga

“Pandu shabdena swetatwa mabhideeyate:

(Dalhana on S.Su.33/23)

Dalhana, the commentary on susrutha samhita, started that pandu means white

colour.

“Pandutwam teshu chaditam yato ataha pandurityuktasa rogaha”(A.H.Chi. 13/13)

Excessive colour of pandutwam is seen in panduroga

“Sarveshu chiteshyapi pandu bhavo yato adhikaha khalu panduroga”(Su. Uttara 44/4))

Excessive pandu varnam is seen in pandu roga.

“Panduhu swetavarna ketakidholi sannibha peetabhagarda varnabhedcha”(Shabdasthoma)

Pandu has been compared with ketaki dhooli or ketaki pushpa colour i.e. thatcan be considered as combination of white and yellow colours.

It can be concluded basing on the above that the disease has been regarded as an

ailment associated with colour of patient.

SYNONYMS OF PANDU ROGAThe synonyms of pandu roga available from vedic literature are vilohita, harima,

halima.

Ref – Adharvana Veda 4-9-3-, 1-22-22)

“Sa kamala panaki pandu roga kumbahwaya laghavakoalasakya vibhashyatelakshana masya kristam nibodha vakshyamyanu poorvashasthoth”

(Su.Uttara 44)

Susrutha used the terms Kamala, Panaki, Panduroga, Kumbahwayo,Laghavaka, Alasaka as synonyms of the disease.

Definition: The word Anemia is derived from two words ‘an’ which means with or

less and “emia” which means blood condition. Pandu (Anaemia) is a condition of

reduction in the haemoglobin concentration of the peripheral blood below the normallevel in relation to age and sex.

These condition of white and yellow colors in equal proportions are called

panduvarnam.

Normal adult male – 16 gms/dl

Normal adult female – 14 gms /dlAnaemia is also said to be present in adults if the "Hematocrit (packed RBC) is

less than 41% in males and 37% in males. Anemia is also seen in patients in whom the

RBC is less than the normal.

Normal adult male RBC – 5,20,000/cumm.

Normal adult female RBC – 4,700,000/cumm

References:l Charaka sutra sthanam 18/42

l Madhavanidanam

l Amarakosha

l Susrutha suthra stana 33/23 – Dalhana commentary uttara sthana – 44/4

l Astanga hridaya Chikitsa sthana – 13/3

l Sabdarnavam,

l Shabda sthoma mahanidhi

CLASSIFICATION OF PANDU ROGA

The pandu roga description available as old as from vedic literature. In vedic

literature there is no evidence of any classification regarding pandu roga. Only

synonyms such as Harima, Halima, Vilohita are found on the literature.

The detail description of pandu roga and is classification starts from Ayurvedic

samhitas only. The classification of pandu roga most of the acharyas accepted 5 types.

Those are 1. Vataja (2) Pittaja (3) Kaphaja (4) Sannipathaja

(5)Mrudbhakshanaja. But susrutha mentioned only 4 types. He excluded the

Mridbhakshanaja pandu and he explained for this as Mridbhakshanaja pandu may

include in vatadi doshaja pandu’s according to the rasa pradhanata of mrit1.

In Haritha samhita “Rukshana” pandu is appears of mridbhakshanaja pandu. The

term Rukshana may be used, because mridhbhakshanaja pandu mainly cause the

Rukshanatwa of the body2.

Astanga sangrahas and many other texts followed the same order while susrutha

mentioned four types.

Some commentators classified Pandu into eight types as follows:

1. Vataja 2. Pithaja

3. Kaphaja 4. Sannipataja

5. Mritbhakshanajanya 6. Sakhasrita kamala

7. Koshtasrita kamala 8. Haleemaka

A Classification states that Mritbhaskhanajanya Pandu falls under sannipataja

Pandu because of the following reasons.

Intake of Kashaya rasa predominant Mrit leads to Vataja Pandu

Intake of Kshara rasa predominant Mrit leads to Pittaja Pandu

Intake of Madhura rasa predominant Mrit leads to Kaphaja Pandu

Probably this may be the reason why Susruta included Mritbhaskhanajanya

Pandu under Sannipataja Pandu.

Classification of pandu according to different authors

S.No Types Vata Pitta Kapha Tridosha Mritbhakshanaja

1 Charaka 5 + + + + +

2 Susrutha 4 + + + + -

3 Vagbhata-1 5 + + + + +

4 Vagbhata-2 5 + + + + +

5 Madhavakara 5 + + + + +

6 Sarangadhara 5 + + + + +

7 Bhavaprakasa 5 + + + + +

8 Haritha 5 + + + + Rukshana

9 Yogaratnakara 5 + + + + +

10 Basavarajeeyam 5 + + + +

11 Vaidhya chintamani 5 + + + + +

MODERN ASPECT

Classification:

Classification of anaemia is 2 types

1. Pathophysiologic classification

2. Morphological classification

1. Pathophysiology classification (Based on Etiology)

1. Anaemia due to blood loss: This has further two types

Blood loss: 1. Acute haemorrhage

2. Chronic Haemorrhage

2. Anaemia due to impaired red cell formation: various causes may produce

this anaemia. These causes are

I. Deficiency of haematinic factors

Ex: A) Iron deficiency

B) B12 deficiency

C) Folate deficiency

D) Protein deficiency

II. Haemopoietic stem cell proliferation differentiation abnormality

Ex: A) Aplastic

B) Red cell aplasia

III. Bone marrow failure due to systemic diseases

A) Anaemia of infections

B) Anaemia of renal diseases

C) Anaemia of liver disease

D) Disseminated malignancy

E) Endo crinopathies

IV. Bone marrow infiltration

Ex: A) Leukaemia

B) Lymphomas

C) Myclosclerosis

D) Multiple myeoloma

V. Congenital anaemia

Eg: A) Sideroblastic anaemia

B) Congenital dyserythropoietic anaemia

III. Increased destruction (Classification of Haemolytic anaemia)

a) Haemolysis (Intransic)

1. Membrane – a) Heriditary spherocytosis

b) Eleptocytosis

2. Haemoglobin a) Sickle cell

b) Unstable haemoglobin

3. Glycolysis Pyruvati kinase etc4. Oxidation G6 PD deficiency

b) Haemolysis (Extrinsic)

1. Immune a) Auto immune

b) Drug toxicity

c) Lympho preliterative disease

2. Morphological classification:

Macrocytic anaemia: In this condition the size of RBC increases i.e. about 94.

Normal is 78-94 as M.C.H. proportionately increased. Eg: Tropical nutritional

anaemia, megaloblastic anaemia of pregnancy, pernicious anaemia1.

Normocytic anaemia: There is reduction in RBC with if all a slight increasing

MCV, MCH remains normal throughout. Eg. Sudden loss of blood due to the

antipartum, post partum haemorrhage2.

Microcytic normocytic anaemia: There is reduction in red cell volume, Hb

content with less MCH eg. Actute and chronic inflammatory disease3.

Microcytic hypochromic anaemia: Reduction in RBC volume and Hb content

and reduced MCH4.

Eg: Iron deficiency anaemia.

References:

1. Susrutha samhita uttarastana 44th chapter

2. Haritha samhita truteeya stana 8 th chapter

3. Charaka samhita sutra 18th, chikitsa 16th chapter

4. Susrutha samhita uttarastana 44th chapter

5. Astanga hridaya nidana stanam 13th chapter

6. Astanga samgraha nidana sthana 13th chapter

7. Madhava nidana 8th chapter

8. Bhavapraksha medhyamakanda II volume

9. Sarangadhara samhita

10. Yogarathnakaram madhymakhandam Vol I pandu roga prakarana

11. Haritha samhita truteeya stana 8th chapter

12. Basava rajeeyam panchama prakarana

13. Text book of pathology, by Byoid

14. Hand bood of human physiology

15. Medicine for students by Dr. Golwalla, 15th Edition

16. Davidson’s principles and practice of medicine – 15th Edition

SHAREERA RACHANA AND KRIYA

“Dosha Dhatu Mala Moolam Hi Shareeram”

Human body build up three doshas, seven dhatus and trimalas. Any disease

occurs the vitiation of dosha, doshyas from their normal functions.

I. The Doshas involved in the samprapti of pandu roga are:

1. Vyanavata

2. Samanavata

3. Pachaka pitta

4. Rajakapitta

5. Bharajaka pitta

6. Kledaka kapha

II. The Dhatus are involved in Pandu Roga are:

1. Rasa 2. Rakta

3. Mamsa 4. Medas

5. Asthi 6. Majja

III. Other factors:

1. Agni 2. Ojas

3. Yakrit 4. Pleeha,

5. Hridaya 6. Raktadharakala

7. Raktaasaya 8. Amasaya

8. Saraktamedas

Since the anatomical and physiological aspect of the above mentioned factors is

important in the study of the pandu roga. Abrief description of the above factors is

needed.

Doshas:1. Vata

a. Yyanavata:

Location: Hridaya – Seat of vyanavata (Vagbhata)

Charaka and Susruta did not mentioned about the place of Vyanavata.

Gunas:

In general, it possesses all the gunas of vayu. They are ruksha, laghu, seeta,

khara, sookshma, and chala.

Karmas:

i. Locomotion is entirely dependent on Vyana Vayu

ii. Rasa Raktadi samvahana

iii. Sweda & Asrik sravana.

iv. Sareera Chestha: Prasarana, akunchana, vinnamana, unnamana and

tiryaggamana

v. Jrimba pravartana

vi. Anna aswadana

vii. Sroto vishodhana

viii. Dhatu tarpana

b. Samanavata: The Vayu that gives strength to Pachaka pitta is called samana

vayu.

Location: It resides near pachaka pitta. It courses between Amashaya and

Pakwashaya. It is also been said that it also occurs in Sweda, Rakta, and Ambu vaha

srothas.

Gunas: In general, it possess all the gunas of vayu.

Karma: The important function of Samana Vayu is to strengthen Jataragni. Thus

it helps in the digestion of food. After digestion, it divides ahara into saara and Kitta

bhaga. According to Vagbhata, samana vata does ahara graham (accepts food) into

koshta, anna grahana, Saara-Kitta vibhajana and it pushes the Kitta into Pureesha vaha

srothas.

2. Pitta

a. Pachaka Pitta: We know that the entire body depends on the food we

consume and the way it is absorbed and assimilated into the body tissues. The type of

pitta that does the above said functions is dependent on Pachaka pitta. This pitta also

regulates digestive capacity, Dhatu parinama and provides nutrition for the body. This

is called as Pachakagni, Koshatagni, Antaragni, Kayagni, Jataragni or Agni,

depending upon the context. It has also been said that vitiation of pachaka pitta leads

to disease.

Location: Pachaka pitta is located in between Amashaya and Pakwashaya. The

region between amashaya and pakwashaya is termed as Grahani and it contains

Pittadhara kala. In other words, Pittadhara kala or Grahani is seat of Pachaka Pitta.

Gunas: Laghu, Vishra, Sara, Dravam, Sneha, Teekshna, Ushna, and Visada

Rasas: Amla and Katu

In Pachaka pitta, the tejo guna predominance is seen and because of it, the

dravatwa guna in pachaka pitta is less when compared to other pittas.

Karma: It has wide range of fuctions. The important functions among them are

as follows:

i. It digests the four types of food and liquids we consume.

ii. It differentiates Saara bhaga and Kitta bhaga of the food after digesting it

and absorbs into the body.

iii. It is termed as ‘Jatara Agni’ many times, because it controls the action of

other 12 types of agni in the body.

iv. The other factors that are dependent on the action of Pachaka pitta are

given below.

A. Ojas B. Ayu.

C. Deha pushti D. Bala

E. Utsaha. F. Health in general

G. Colour of skin

It is also said that if Kayagni is healthy, then the person achieves longevity, else,

he acquires diseases and if the Kayagni is totally destroyed, the person dies.

b. Ranjaka Pitta.

The pitta that is transforms rasa dhatu into rakta dhatu is called Ranjaka pitta or

Ranjakagni pitta.

“Amasayaasryayam Pittam ranjakam rasaranjanath” (A.H.S. 12-12)

Location: According to Susruta - Yakrit and pleeha

According to Vagbhata – Amashaya

According ot Sarangadhara – Hridaya

Gunas: Same as that of pachaka pitta

Karma: Ranjaka pitta gives colour to the Rasa Dhatu when it is circulated

through Yakrit and Pleeha and transforms it into Rakta Dhatu. This act is even

controlled by Rakta Dhatwagni.

c. Bharajaka Pitta:

The temperature of the body as well as the colour of the skin are dependent on

Bhrajaka pitta.

“Twakstham bhrajakam bhrajana twachaha” (A.H.S. 12-14)

Location: Skin is the site of Bhrajaka pitta. Avabhasini, which is the first layer

of skin, lodges Bhrajaka pitta according to Dalhana.

Gunas: Same as pachaka pitta.

Karma:

i. The main action of Bhrajaka pitta is to manintain temperature of the body.

ii. In general, Bhrajaka pitta gives different colours to the body depending upon

the Mahaboota composition of the skin.

According to Charaka

Jala & Akasa Mahabhoota predominance leads Goura Varna

Pridhvi Mahabhoota predominance leads Krishna Varna

Pridhvi & Akasa Mahabhoota predominance leads Krishna Syama Varna

According to Susruta:

Jala & Akasa Mahabhoota predominance leads to Gowra Syama Varna

iii. It reflects different characteristics of body in health and diseased states.

iv. It absorbs the oils or medicines applied over the surface of the skin, in the

form of Abhyanga, Parisheka, Avagahana and Lepana.

3. KAPHA

Kledakakapha

Location: The site of kledaka kapha is Urdhwa Amashaya

Gunas: In general, it possesses all the gunas of Kapha such as Shingdha, Seetha,

Guru, Manda, Slakshna, Sandra, and Sthira.

Karma: 1. Anna sanghata 2. Kledana

The impirement of these functions are supposed to vitiate ahara which may result

into Pandu.

Dhatus

The Dhatus that are involved in the pathogenesis of Pandu are Rasa, Rakta,

Mamsa and Meda as per several authors.

Rasa Dhatu: The involvement of rasadhatu is not directly related in the

Pathogenisis of Pandu roga samprapti. Pandu is included under rasa prodoshaja

diseases.

Location: Hridaya and Dasadhamanis. It circulates through out the body along

with Rakta with the help of Vyanavatha.

Pramana: 9 Anjalis

Rasa: Madhura

Varna: Swetha/Sukla

Formation: It is formed from Saarabhaga of ahararasa after it has been subjected

to jatarapaka and Rasadhatwagnipaka. It stays in each dhatu for a period of 3015

kalas. It circulates upwards like Agni, downwards like jala and transversely like

shabda.

Karma: 1. Tarpana 2. Jeevana & Preenama 3. Vardhana 4. Dharana

5. Yapana 6. Uttaradhatu poshana

Rakta Dhatu:

According to the Ayurvedic view, Rasadhatu contributes to the formation of the

rakta dhatu with the help of Ranjaka pitta. Therefore the Ranjakapitta plays an

essential part in the formation of the Raktadhatu.

“Tejo Rasanam sarvesrham manujanam yaduchyathe”

Pittoshmanahasia Ragena Raso Raktatramrucchati

The etiological factors of Raktadusti are similar to the Panduroga etiological

factors. The characteristic features of Pandu quite opposite to the characters of

Shuddharaktapurusha. The Pandu roga is mentioned under Rakta kshaya lakshanas.

“Yathu Yakritpleeho pittam Tasmin ranjakognirthi sangna

Sa Rasasya Ragakruduktha ha”

Location: Yakrit, Pleeha, Hridaya, Rakta vahadhamanis and Sarakta medas. It

circulates in the entire body along with rasadhatu.

Pancha bhoutika Sangatana of rakta:

“Panchabouthikam twapare Jeevarakta maharacharyaha

Visratha Dravatha Ragada spandanam Laghuta tatha

Bhumyadenam guna hothe drushanthe chatra shonita

Qualities of Rakta dhatu Bhuta Pradhanyatha

1. Visratha (Fleshy odour) Prodhweebhuta

2. Drava (Fluidity) Jalabhuta

3. Raga (movement) Agnibhuta

4. Spandhana (movement) Vayubhuta

5. Laghuta (lightness) Aakashabhuta

Rasa: Madhura/Madhura lavana rasas.

Varna of suddha rakta dhatu:

“Tapaniyendra Gopabham padmalaktaka sannibham

Gunjaphala savarnacha vishuddam vidhisonitham”

The pure blood looks lika a bright “Indragopa”

Looks like Padma (Lotus flower) and Latuka (Laksha)

Gunjaphala Savarnam – Brightly red like gunja seed. These colour indicative of

pure blood.

Pramanas: Eight Anjalis.

Gunas: Anushna, Seetha, Snigdha, Guru, Visra and Asamhata and Gunas of

Panchamahabhutas.

Karma: Jeevana, Dharana, Bala, Varna, Sukhakara, Ayushkara, Pushtikara,

Indriyaprasannatwa, mamsapushti and sparshagnanakara.

Shuddha Raktasaara Purusha Lakshanas: A person whose karnamukha,

jihwa, nasa, osthta, pani, paadatala nakha, lalata and mehana are having snigdha and

rakta Varna is regarded as Shudda Raktasaarapurusha.

Ojus:

The involvement of ojus is specifically mentioned in Charaka Chikitsa 16th

Chapter. As the formation of all Dhatus is impaired in the disease Pandu, the

formation of the essence of all Dhatus also impairs and ojokshaya lakshanas are seen.

Location Hridayam, Sarva shareeram

Types Para and Apara

Pramana Para Ojus – Asta bindu

Apara Ojus – Ardhanjali

Rasa Madhura

Varna Eshatpeeta varnam (or) Sarpivarnam.

Karma Balakaram, Vyadhi kshamatwakaram, Tushtikaram,

Pushtikaram, and it is associated with Ayu (life).

MODERN ASPECT

The circulatory system is the transport system that supplies O2 and substances

absorbed from the gastrointestinal tract to the tissues, returns CO2 to the lungs and

other products of metabolism to the kidneys, functions in the regulation of body

temperature, and distributes hormones and other agents that regulate cell function.

The circulatory (or) vascular system is divided for descriptive purpose into two

main parts

1. The Lymphatic system

2. The Blood circulatory system

The Disease pandu roga is similar to the disease 'Anaemia' of modern

medicine. Anaemia is concerned with lower haemoglobin levels in the blood. It is a

condition in which the oxygen carrying the capacity of the blood is reduced.

The blood: Blood is described liquid as a connective tissue. It acts as communication

between the cells of different parts of the body and the external environment. Blood:

constitutes 7% of the body weight. It is about 5-6 liters.

Other Physical characters of blood:

Viscocity – 4.5-5.5 (higher than water)

Temperature – About 380C ( Slightly higher than normal body temperature

PH-range – 7.35 to 7.45

Total blood volume – 72-10ml/kg body weight.

Composition of the blood:

Microscopically blood is composed of two parts.

1. Blood plasma: Contains dissolved substances (55%), water, plasma proteins

clotting factors, inorganic salts, nutrient materials, hormones, enzymes, antibodies and

gasses.

2. Formed elements: Contains cell and cell fragments (45%) – Red blood cells or

Erythrocytes, white blood cells or leucocytes and platelets or thrombocytes present

less than 1% of the total blood volume.

Formed elements: The element of the blood are:

1. Erythrocytes (Red blood cells)

2. Leucocytes (White blood cells)

I. Granular leukocytes (Granulocytes)

a. Neutrophils

b. Eosinophils

c. Basophils

II. Agranular leukocytes (Agranulocytes)

a. Moconcytes

b. Lymphocytes (T cells, B cells and Natural killers)

3. Platelets (Thrombocytes)

ERYTHROCYTES (The red blood cells)

Erythrocytes: Of all the cells of the body RBCs are most abundant. The major

Function of RBC also known as erythrocytes is to transport haemoglobin, which in

turn carries oxygen from lungs to tissues. Haemoglobin is present in RBC in humans.

RBC have other functions besides transport of hemoglobin. They contain large

quantities of carbonic anhydrase, which catalyses the reactions between water andCO2, increasing the rate of this reversible reaction to as much as several thousand

times. This makes it possible for water in blood to react with huge CO2 and thereby

transport it to lungs from tissues in the form of BiCarbonate Ion (HCO3).

The Haemoglobin in the cells is an excellent Acid – Base buffer and is

responsible for most of buffering power of whole blood.

Size and shape of RBC: Normal RBCs are bioconcave discs having a mean

diabmeter of about 7.8 m and a thickness of about 2.5 mm at the periphery and 1mm

of less in the center. The shape of RBCs can change remarkably as the cells pass

through capillaries.

Concentration of RBCs in the blood: The average volume of the red blood

cells is 83 cubic micrometer

In normal men - 5,200,000 (+/- 300,000)

In normal women – 4,700,000 (+/- 300,000)

Quantity of Hb in the cells: RBCs can accommodate 34 gms/dl of Hb in the cell

fluid, when the heamatocrit ( the percentage of blood that is in the cells- normally 40

to 45%) and the quantity of haemoglobin in each respective cells are normal. The

whole blood contains an average of Haemoglobin in

Men – 14-16 gms/dl

Women 12-15 gms/dl

Infants – 14-20 gms/dl

Each gram of pure Hb is capable of combining with about 1.39 ml of oxygen.

In normal man, Hb/dL of blood carries more than 21 ml of O2.

In normal women, Hb/dl of blood carried more than 19ml of CO2.

PRODUCTION OF RBC AS PER AGE:

l Yolk Sac: In early few weeks of embryonic life – primitive nucleated RBC areproduced.

l Liver spleen & Lymphnodes: During mid trimester of gestation – the liver isthe main organ or production of RBC, although ressonable number of RBC areproduced by spleen and lymph nodes.

l Bone marrow: During the last months of gestation – RBC are producedexclusively from bone marrow.

l Upto 5 years – Bone marrow of all the bones produces RBC.

l After 20 years – Long bones stop prodcing RBC since fatty tissues occupymost of the cavity. Beyond this age RBCs are produced by marrow ofmembraneous bones such as verterbrae, sternum, ribs and ilia.

Origin and development of Red Blood Cells: The first cell that can be

identified as belonging to the red blood cells series is the proerythroblast. Once the

proerythroblast has been formed, It divides several more times, eventually forming

many mature red blood cells. The first generation cells are called Basophilic

erythroblasts, which then develops into a Proerythroblast (Normoblast) erythroblast,

the first cells in the sequence that begins to synthesize hemoglobin. The poly

chromatophilic erythroblast next develops into an acidophilic erythroblast, in which

hemoglobin synthesis is at a maximum. In the next stage, the acidophilic erythroblast

ejects is nucleus and becomes a reticulocyte. The reticulocyte in turn becomes an

erythrocyte (or) mature red blood cell. Once the erythrocyte is formed, it leaves the

marrow and enters the blood stream.

Formation and destruction of red blood cells and recycling of hemoglobin

components.

Red blood cells live only about 120 days because of the wear and tear inflicted

on their plasma membranes as they squeez through blood circulation worn-out red

blood cells are removed from circulation and destroyed by fixed phagocytic

macrophages in the spleen and liver. The globin and heme protions of

hemoglobin are split apart. Globin is brokendown into amino acids, which can be

reused to synthesize other proteins. Iron removed from the heme portion. Associates

with a plasma protein called transferring, which transports iron in the blood stream. In

muscle fibers, liver cells, and macrophages of the spleen and liver, iron detaches from

transferring and attachs to iron storage proteins called ferritin and hemosiderin.

Upon release from a storage site or absortion from the gastrointestinal tract, iron

attaches to transferring. It is then transported to bone marrow, where RBC precursors

take it up through receptor – mediated endocytosis. For use in production of new

hemoglobin molecules. Erythropoiesis in red bone marrow results in the production of

red blood cells, which enters the circulation.

At the same time, the non-iron protion of heme is converted to biliverdin,

agreen pigment, and then into bilurubin, an orange pigment. Bilurubin enters the

blood and is transported to liver with in the liver, bilirubin is secreted by liver cells

into bile, which passed into the small intestine. Again which passed into the large

intestine, in large intestine bacteria convert bilurubin into urobilinogen. Some

urobilinogen is obsorbed back into the blood, converted to urobilin, a yellow pigment,

and excreted in urine. Most urbilinogen is eliminated in feces in the form of a brown

pigment called stercobilin, which gives feces their characteristic colour.

Erythropoietin: The principal factors that the stimulates red blood cell production is

a circulating hormone called erythropoietin.

Tissues oxygenation is a basic regulator of RBCs production. Any condition that

causes the quantity of oxygen transported to the tissues to decrease ordinarly increase

the rate of RBCs production.

Other factors controlling erythropoises: The red cells are constantly being

destroyed and regenerated. Certain factors are necessary for the formation of red

blood cells. They are:

1. Diet: Proteins are very valuable supply of essential amino acids for the synthesis of

hemoglobin.

2. Metals: Iron, Copper, Cobalt, Calcium and Manganese. Iron is essential for the

formation of hemoglobin. Copper, Cobalt, Calcium and Manganese are indirectly

helpful in the formation of RBCs.

3. Bile satls: Presence of bile salts in the intestine is essential for the proper absorption

of these metals.

4. Endocrine glands: Certain glands such as thyroid and adrenal glands are having

unknown role in the metabolism of RBC.s

5. Vitamins: Vitamin C, B complex, and Folic acid are helpful in the formation of

RBCs.

Erythropoietin and its formation: Erythropoietin is a hormone found in circulating

blood. It is a glycoprotein with molecular weight of 34,000. In the absence of

erythropoietin, hypoxia has little or no effect in stimulating RBCs production. On the

other hand, when Erythropoietin system is functional, hypoxia causes marked increase

in Erythropoietin production, and this in turn enhances RBCs production until hypoxia

is relieved.

Role of kidneys in the formation of erythropoietin: In normal person, about 90% of

all erythropoietin is formed in the kidneys. Mainly, the liver forms the remainder. The

renal tubular epithelial cells secrete the erythropoietin because anemic blood is unable

to deliver enough oxygen from peritubular capillaries to the highly oxygen –

consuming tubular cells, thus stimulating erythropoietin production.

Effect of erythropoietin on erythrogenesis: The important effect is to stimulate the

production of proerythroblasts from hemopoietic stem cells in the bone marrow. Once

the proerythroblasts are formed, the erythropoietin causes these cells also to pass more

rapidly through the different erythroblastic stages than normal, further speeding up the

production of new cells. The rapid production of cells continues as long as the person

remain in low oxygen state or unitl enough RBCs are producted to carry adequate

amounts of oxygen to the tissues.

Formation of RBCs – Requirement of Vitamin B12 and Folic Acid: For the final

maturation of RBCs, two vitamin – B12 and Folic acid are very imporntat. Both of

these are essential for the synthsis of DNA, because each in a different way is required

for the formation of Thymidine Triphosphate, an essential building block of DNA.

Therefore, lack of either of these causes diminished DNA and consequently, failure of

nuclear formation and division. Therefore, it is said that Vit. B12 and folic acid

deficiency causes ‘maturation failure’ in the process of erythropoiesis.

Folic Acid: The normal concentration range of folic acid in blood is 5-15 mg/ml. It is

found mainly in green vegetables, liver and whole grains. The reference nutrient

intake is 50g/day. Following its uptake by the mucosal cells, folate undergoes

reduction and methylation. Once, it arrives in the liver, the methyl derivative is taken

up, undergoes demethylation and the tetrahydrofolate is converted into polyglutamyl

forms with 4,5 or 6 residues. The polyglutamyl forms contstitute a store of the

vitamin. Prior to release from the store, and into the circulation, the compound is

converted to N-methyl-derivative, from which all but one of the glutamyl residues is

removed.

Folate deficiency: The members of society most liable to folate deficicney are

pregnant women and the elderly. It is now recognized as being good practice to

administer folate supplements as soon as pregnancy is confirmed and to continue until

term. In the first trimester the supplementation in prophylactic, benefiting the foetus,

because there is clear evidence that the occurance of neural tube defects such as Spina

bifida and anencephaly is reduced by as much as two-thirds. Later in the pregnancy

the supplementation is to prevent folate deficiency in the mother, which can easily

arise as foetal demands cause depletion of maternal foliate stores.

Less commonly, folate defienciey may be seen in alcoholics, in those patients

being treated with anticonvulsants and in individuals with intestinal malabsorption

conditions.

VITAMIN B12: Normal daily requirement of Vitamin B12 is 1-2 g/day. It enters into

food chain only in food of animal origin. The acid conditions and the proteinhydrolysis that commences in the stomach jointly cause the release of Vitamin B12. In

saliva and also in gastric secretions are a group of mucins, termed R-Binders.

These glycoproteins bind vitamin B12 with high affinity in the acid environment of the

stomach. In the more neutral surroundings of the duodenum the R-binders undergo

hydrolysis, thereby releasing their Vitamin B12.

Intrinsic factor: Maturation of the cell depends on a number of factors, especially the

presence of vitamin B12 and folic acid. These are present in sufficient quantity in a

normal diet. Containing dairy products, meat and green vegetables. If the absorption

of vitamin B12 depends on a glycoprotein called intrinsic factor secreted by parietal

cells in the gstric mucosa. Thus very little or none is absorbed in cases with pernicious

anaemia and after gastrectomy as the intrinsic factor absent. In main it is produced by

the body of the stomach. It is glycoprotein.

The essential property of the intrinsic factor is its ability to bind Vit B12 and to act as

a carrier. The presence of hydrochloric acid probably facilities this binding in the

stomach only the vitamin B12 part enter blood to be transported to red bone marrow.

Process of absorption:

1. The intrinsic factor binds tightly with Vit.B12 and in this bond state, Vit.

B12 is protected from digestion by the gastro intestinal enzymes.

2. Still in the bond state, the intrinsic factor binds to specific receptor sites on

the brush border membranes of the mucosal cells in the ileum.

3. VitB12 is transported into the blood by the process of pinocytosis carrying

the intrinsic factor and vitamin together through the membrane. This is a

process that is dependent on Ca.2+.

Lack of intrinsic factor, therefore causes loss of much of the vitamin, because

of both digestive enzyme action in the gut and failure of its absorption. The transport

of Vitamin B12 in the plasma occurs in association with two major binding

proteins:Transcobalamin I and Transcobalamin II.

IRON METABOLISM:

Metal ion used most frequently in association of proteins often include iron in

their structures (sometimes copper, occasionally manganese).

The use of iron as the metal in biological systems for this purpose seems, in part,

to have arisen due to its great abundance in the environment. It has greater affinity for

already association with, and dissociation from its binding sites on protein i.e., its

kinetic liability. The complexes formed, however, are thermodynamically stable. The

major iron-bearing proteins in the body are not enzymes, however, but the dioxygen-

binding and dioxygen-transport proteins myoglobin and hemoglobin.

1. Sources: All animal food eg. Meat, liver, egg etc., excepting milk and butter.

Vegetables, eg: peas, lentils, green leaves, fruit.

2. Iron intake: In the normal population, requirements for iron replacement range

from 1.0 to 3.2 mg/day, and this must derive from, dietary srouces/Although iron is

widely distributed in foodstuffs, only a proportion, which may be 10% or less, is

absorbed from the diet. For this reason, the minimal amount needed to be ingested

daily is set at 10 times the amount actually lost daily.

3. Absorption and transport: Iron is absorbed mostly from the whole of the gastro-

intestinal tract but a large amount is absorbed from the upper part of the small

intestine particularly the duodenum. Dietary iron is absorbed through the mucosal

cells as Ferrous (Fe++) form. Iron in diet is mostly present as a ferric (Fe+++) state

which is reduced to ferrous form during absorption. Vitamin C, glutathione and amino

acid – SH groups help in reduction of ferric to ferrous form. After entering the

mucosal cell as Ferrous form, the iron molecules are rapidly reconverted into ferric

state. A ferric iron as ferric – hyroxy phosphates combines with a protein, apoferritin

with a protein apoferritin of. The mucosal cells with the formation of iron-phosphorus

protein complex, ferritin, This ferritin is one of the storage forms of iron in the tissue.

4. Absorption of iron depends upon the factors: The acidity of the gastric juice

helps absorption. The gastric HCL helps reduction from ferric form to ferrous. Partial

gastrectomy often leads to iron deficiency anaemia. Calcium small amount decreases

the formation of insoluble iron phosphates and thus helps absorption but large amount

of Ca. inhibits iron assimilation. Vitamin – C increases the absorption of iron from

foods, possibly reducing the ferric iron into the ferrous state.

5. Time taken for absorption: The rate of absorption is determined by the iron

requiremen for Hb synthesis. In anaemic cases, after a single dose of iron, a rise of

serum iron takes place in 30 minutes, reaching its maximum in 3-5 hours and returns

to normal in about 12 hours. Maximum absorption is completed in 18 hours.

6. Iron storage: iron is incorporated into the iron-storage protein Ferritin, in

enterocytes, but the main stores of iron in the mammalian body are in the liver and

spleen. In addition to storage as Ferritin, iron can also be found in a form called

Haemosiderin inside the liver.

7. Iron balances: For an adult to stay healthy, the amount of iron lost each day much

be replaced by an equivalent intake. Young rapidly growing children, on the other

hand, will require a positive iron balance. The factors that influence daily iron loss,

daily iron intake and absorption from the gastrointestinal tract are to be mostly

considered.

8. Iron excretion: Iron is unique among the trace elements in that there is no

excretory system for eliminating the metal from the body. This is generally lost

through erythrocytes in bleeding. The routes for loss of iron may be classified as

either physiological or pathological.

9. Physiological Iron Losses: The adult male and the non-menstruating female lose

about 1 mg iron per day. Of this total, 50-60% is accounted for by loss from the

gastrointestinal tract, due either to biliary excretion or to the shedding of mucosal

cells. The remainder is lost with hair, sloughing of skin or in the urine. Lossess during

menstruation typically range, on average, from 1.4 to 3.2 mg Iron per day.

Losses associated with underlying pathology: A range of conditions give rise to

blood loss, but is appropriate to discuss this under Nidana.

10. Function of iron: (a) Formation of haemoglobin (b) Development of red cells (c)Oxygen carriage in blood (d) Related to tissue oxidation (e) Supplies O2 to the

muscles (f) Relation with cell nucleus and oxidation in nerver cells.

11. Deficiency signs: Iron deficiency causes secondary anaemia.

Haemolysis: By the term haemolysis is meant the disrutption of red cells with the

escape of haemoglobin from the corpascles to the plasma. Blood may be haemolysed

in the different ways:

1. By adding fact solvents – Ex: Ether, chloroform, benzene etc

2. By causing osmotic disturbance

3. Disturbing the surface tension – addition bile salts

4. Physical methods – Alternate freezing and thawing of blood breakdown

RBC

5. Mechanical – vigorous stirring and shaking

6. Addition of incompatible blood – Agglutinates the red cells.

7. Adding bacterial haemolysis

8. Adding snake venom (viper)

9. Drugs: like quinine, phenacetin, nitrates, chlorates etc.

Leucocytes (The White blood cells)

They are largest blood cells. They contain nuclei and some have granules in their

cytoplasm. White blood corpuscles are an important variety of cells in the blood.

These cells differ from the red cells in many respects. For instance.

(1) They do not contain any haemoglobin

(2) They are bigger in size

(3) They are nucleated, living cells.

(4) They are actively amoeboid

(5) They are much less in number

(6) Their span of life is shorter.

(7) Their origin is purely from extravascular tissue

(8) Their functions are absolutely different from those of red cells.

(9) There are several varieties of leucocytes, where as red cells are only one

variety. Normal leucocytes count – 4000-11000/cumm.

Classification and differential count of Leucocytes:

The classification and differential count as generally accepted two major groups:

1. Granulocytes Polymorphonuclear leukocytes)

Consequently this group includes three varieties:

A) Neutrophil

B) Eosinophil

C) Basophil

2. Agranular leukocytes (A granulocytes)

Two varieties

A) Lymphocytes

B) Monocytes

Again lymphocytes 3 types

A) T – lymphocytes

B) B- lymphocytes

C) Natural killer cells

(I) Granulocytes: These cells originate from stem cells (haemocytoblastas) in red

bone marrow and go through several developmental stages befor entering blood, a

process called granulopoiesis. They follow a common line of development through

myeloblast before differentiating into the three types. Their names represent the

dyes they take up when stained in the laboratory. Eosinophils take up the red acid dye,

basophiles take up the blue; and neutrophile are purple because they take up both

dyes.

(A) Neutrophils: Neutrophil is about 10-12m in diameter. Most numerous in the adult

blood, about 60-70%. The necleus is many-lobed; the number of lobes varies from 2

to 7 or more. Neutrophils have limited life span of around 12-24 hours in the blood.

Their main function is to protect against any foreign material that gains entry to the

body. Mainly microbes, and to remove waste material. They are attraced in large

numbers to any area of infection by chemical substances, released by damaged cells,

called ‘Chemotaxins’. Neutrophils pass through the capillary walls in the infected area

by amoeboid movement. There after they ingest and kill the microbes by a process

called “Phagocytoses”.

(B) Eosinophils: Eosinophils is 10-12 m in diameter. Eosinophils are charecterised by

their two-lobed. Nucleus they have significant proinflammatory and cytotoxic activity

and play a role in the pathogenesis of various allergic, parasitic and neoplastic

disorders. The eosinophils are amoeboid but not phagocytic. Eosinophils is about 2-

4%. The most common causes of eosinophilia in the world are allergic disorders such

as asthma, eczema and high fever. In developing contries parasitic infections are

frequently implicated. Other relatively common aetiologies are drug hypersensitivity,

various skin disease and connective tissue disorders.

(C) Basophils: Basophils is about 8-10m in diameter. The nucleus is kidney shaped.

The cytoplasm contains a large numbers of round granules which take deep basophilic

stain. Basophils are the least numerous of the blood leucocytes. Basophils secrete

histamine which causes vaso dilatation and increases the permeability of capillary

walls. Basophils and their tissue equivalent, most cells, have receptors for the protion

of I g E. They play a central role in immediate hypersensitivity reaction. Basophils

is usually associated disorders Eg. Chronic myeloid leukaemia. However it may be

reactive to a range of systemic diseases including inflametory bowel disease and

hypothyroidism. Basophil count about – 0.5-1%.

(2) A granular leukocytes (Agranulocytes): The type of leukocyte with no granules

in their cytoplasm are monocytes and lymphocytes.

(A) Monocytes: These are large mononuclear cells that originate in red bone marrow.

Monocytes are 16-18mm in diameters. Monocytes developed from monoblasts. Some

circulate in the blood and are actively motile and phagocytic, while others migrate into

the tissues where they develop into macrophage.The macrophage system, some time

called the lymphoreticular system, consisits of fixed pahgocytic cells which multiply

in situ. These cells are found in a wide variety of tissues. Eg.

Histocytes in connective tissue,

Microglia in the brain.

Kuffer cells in liver sinusoids.

Alveolar macrophages in the lungs.

Sinus – living macrophages in the spleen,

Lymphnodes & Thymus gland

Mesangial cells in glomerulus of nephron in the kidney.

Osteoclats in bone.

Monocytopenia is less frequently noted but can be severe in patients receiving

cortico steroid treatment. Monocytes count – 3.8%.

Lymphocytes: Lymphocytes are developing from haemocytoblasts in red bone

marrow. Lymphocytes are associated with protection of the body against foreign

material. Lymphocytes are spread in the blood stream to lymphoid tissue else where in

the body where they are activated i.e. they become immunologically competent

which means they are able to respond to antigens (Foreign material). Lymphocytes

count about 20-25%.

The major types of lymphocytes are T-lymphocytes, B-lymphocytes and natural killer

cells.

A. T. Lymphocytes: T.Lymphocytes, activated by thymosin in the thymus gland.

They are sensitized when they encounter an antigen for the first time. Effector cells

act directly against antigens in conjuction with phagocytes. The main T-lymphocytes

are cytotoxic and are responsible for long-term protection against some viruses,

bacteria, fungi, cancer cells, pollenfrom flowers and platns, some large molecule

drugs Eg. Pencillin. They are also responsible for the rejection of transplanted organs

T.Lymphocytes, which are responsible for cell mediated immunity.

Other T-lymphocytes are helper T cells, which activate B cells, and suppresor T-

cells, which inhibit B cell activity. T. Lymphocytes produce a number of chemical

substances

(A) Lymphokines that attract macrophages to the site

(B) Lymphotoxin that kills foreign cells eg-microbes

(C) Interferons that prevent virus reproduction inside cells.

B-Lymphocytes: B cells are derived from the stem cells of the bone marrow. B-

lymphocytes are responsible for humoral immunity. B.Lymphocytes are activated by

both microbes and their toxins. B-Lymphocytes, which are responsible for humoral

immunity. These are five subclasses IgG, IgA. IgM, IgD and IgE. The antibodies

promote phagocytosis of foreign particles and neutralize toxins.

Variations in normal count of white blood corpuscles:

a) Muscular exercise (asphyxia)

(b) Relation with after meal.

(c) Injection of adrenaline

(d) Emotional stress

(e) Relation with pregnancy and labour

(f) Increased cellular destruction from injections & surgical operations

(g) Asthma, high fever, skin disease

(h) Starvation and administration of certain chemicals like benzene.

Functions of white blood corpuscles:

(a) Phagocytosis

(b) Antibody formation

(c) Formation of fibroblast

(d) Manufacture of trephones (nutrition growth, and repair of tissues)

(e) Secretion heparin

(f) Antihistamin function

(3) Thrombocytes (Platelets):

They are very small non-nucleated discs derived from the cytoplasm of

megakaryocytes in red bone marrow. The normal platelet count is between 2,50,000 to

40,00,000/mm3 of blood. Platelets have a short life span. Normally, just 5-9 days.

Aged and dead platelets are removed by fixed macrophages in the spleen and liver.

Coagulation (Clotting): Normally, blood remains liquid as long as it stays with in its

vessels. If it is drawn from the body, however, it thickness and forms a gel. Eventually

the gel separates from the liquid. The red-coloured liquid called serum. The gel is

called clot. The process of gel formation it called clotting or coagulation. Clotting

involves several substances known as clotting factors:

Clotting factor:S.No. Synonym Source Pathway

I Fibrinogen Liver Common

II Prothrombin Liver Common

III Tissue factor (thrombo plastin) Damaged tissue &

Activated platelets Extrinsic

IV Calcium ions (Ca2+) Diet, bones, and

platelets All

V Proaccelerin, labile factor or

Accelerator globalin (ACG) Liver and platelets Extrinsic &

Intrinsic

VII Serum prothrombin conversion Liver Extrinsic

acceleralor stable factor or

proconvertin

VIII Antihemophilic factor (AHF) Platelet & Intrinsic

Antihemophilic globulin (AHG) Endothelial

IX Christamas factor, plasma Liver Intrinsic

Thromboplastin component (PTC)

Or antihemophilic factors B

X Start factor, power factor, or Liver Extrinsic &

Thrombokinase Intrinsic

XI Plasma thromboplastin Liver Intrinsic

antecedent (PTA) or antihe-

mophilic factor C

XII Hageman factor, glass factor, Liver Intrinsic

Contact factor or antihemophiliac

facrorXIII Firbin-stabilizing factor (fsf) Liver & Platelets Common

There is no factor VI, prothrombinase (prothrombin activator) is a combination of

activated factor 5 and 10.

Haemostasis blood clotting is 3 basic stages

Stage - I

Stage – II

Stage – III

Stage-I : The formation of prothrombinase is initiated by either the extrinsic or the

intrinsic pathways blood clotting.

Extrinsic path way: The extrinsic pathway of blood clotting has fewer steps than the

intrinsic pathway and occurs rapidly, with in a matter of seconds if trama is severe.

Damage to endothelim tissue protein called tissue factor (IF) also known as

thromboplastin or coagulation factor III, leaks into the blood from cells out side

(extrinsic to) blood vessels and initiates the formation of prothrombinase. IF is

mixture with of lipoproteins and phospholipids released from the surfaces of damaged

cell. It activates clotting factor VII, which next combines with factor X, thus

activating it. Once factor is activated, it combines with factor V in the presence of

calcium ions (Ca2+) to form the active enzyme prothrombinase. This completes the

extrinsic pathway.

Intrinsic pathway: The intrinsic pathway of blood clotting is more complex than the

extrinsic pathway. And it occurs more slowly, usually requiring several minutes. IF

endothelial cells (cells in the blood vessel) become roughened or damaged, blood

came in contact with collagen in the surrounding basal lamina, in addition, trama to

endothelial cells causes damage to blood platelets, resulting in the release of

phospholipids by the platelets. Contact with collagen activates clotting factor XII. In

turn, factor XII activates XI which activates factor IX. Activated factor VII (From

extrinsic pathway) also can activate factor IX. Activated factor IX joins with the factor

VIII and Platelets phospholipids to activate factor X. Once factor X is activated it

combines with factor V to form the active enzyme prothrombinase.

Stage2: Once prothrombinase is formed, the common pathway follows. In the second

stage of blood clotting, prothrombinase and Ca2+ catalyze the conversion of

prothrombin to thrombin.

Stage3: In the third stage, thrombin, the presence of Ca2+, converts fibrinogen, which

is soluble to loose fibrin threads, which are insoluble. Thrombin also activates factor

XIII (fibrin stabilizer factor), which strengthen and stabilized the fibrin threads into a

sturdy clot.

- Bleeding time – 2.5 mints.

- Prothrombin time – 11-16 sec

- Clotting time – 6-7 mints.

Blood groups

The surface of erythrocytes contain some glycoproteins and glycolipids that can

act as antigens, are normal components of one person’s RBC plasma membrane that

can trigger damaging antigen – antibody responses in other people. Based on the

presence or absence of various isoantigens. In there are four principal blood groups,

designated O, A, B and AB. These blood groups deffer in the types of antigens that

are present on the erythrocytes. Persons with type A blood have a Aantigens. Those

with type B, B antigens: Those with type AB, both A and B antigens: In addition, the

plasma of group ‘O’ blood contains antibodies to A, B and AB. Group A plasma

contains antibodies to B antigens and group B plasma contains antibodies to A

antigens. Group AB plasma has no antibodies to O, A, or B antigens. In blood

transfusions cross-matching is necessary to prevent agglutination of donor red cells by

antibodies in the plasma of the recipient because plasma of groups A, B and AB has

no antibodies to group O erythrocytes, people with group ‘O’ blood are called

‘Universal doners’. Conversely, persons with AB blood are called Universal

recipients, because their plasma has no antibodies to the antigens of the other three

groups.

In addition to the ABO blood grouping, there are Rh (Rhesus factor) – positive and

RH Negative groups. An RH-Negative person can develop antibodies to Rh positive

red blood cells if that person is exposed to Rh. Positive blood. For example, during

pregnancy a mother who is Rh negative can make antibodies for Rh-possitive cells in

the fetus is Rh positive (inherited for Rh positive). Rh-positive red cells from the fetus

can enter the maternal blood stream at the time of plancental separation and induce

Rh-positive antibodies in the mother plasm. The Rh-positive antibodies from the

mother can also reach the foetus via the placenta, and agglutionate and haemolyze

foetal red cells. This condition is known as Erythroblastosis foetalis, a haemolylic

disease of the new born.

Functions of blood:

1. Transport of respiratory gases. It transports oxygen form the lungs to all cells

and carbondioxid from cells to the lungs.

2. Transport of nutrition from the digestive organs.

3. It transports the waste products from the cells to the kidneys, lungs, and sweatglands.

4. Maintenance of water balance

5. Regulation of body PH and body temperature

6. It protects against toxins and foreign microbes.

7. It transport the enzymes and hormones to the cells

8. Regulation of blood pressure.

9. Maintenance of ion balance

10. It prevents the body fluids loss through clotting mechanism.

References:

1. Charaka Samhita, Sareera Sthana, 7th Chapter

2. Charaka Samhita, Sutra Sthana, 24th and 28th Chapters.

3. Charaka samhita, Vimana Sthana, 5,7,8 Chpater

4. Susruta Samhita, Sareera Sthana, 1st Chpater

5. Susruta Samhita, Sutra Sthana, 14th, 21st, and 42nd chapters.

6. Astanga Hridaya, Sutra Sthana, 1st, 12th, 16th, 20th Chapters

7. Principles of Anatomy and Physiology by J. Tortora.

8. Textbook of Physiology by C.C. Chatterjee.

9. Applied Physiology by Samson Wrights.

10. Textbook of Medical Physiology by Guyton & Hall

11. Human Physiology by Chakrabarti, Ghosh and Sahana

12. Will's Biochemical Basis of Mecdicine.

13. Regional and Applied Human anatomy by Dr. B.D. Chaurasia.

NIDANAThe word panchalakshana nidana indicates that there are five topics to discuss

under this text. It helps a physician to come to exact diagnosis of the disease. They are

I. NIDANA – The etiology

II. POORVAROOPA- The prodromal symptoms signs.

III. ROOPA – The signs ans symtpoms

IV. UPASAYA & ANUPASAYA – The comforting and aggravating factors

V. SAMPRAPTI - The pathogenesis.

NIDANA (Etiology)

Nidana is said to be disease producing factors and they are called as aeteological

factors in modern medicin.

“Seti kartavyatako rogotpadaka Heturn nidanam”

Means the factors, which plays an essential role in causing a disease vividha

ahita ahara vihara which cause vyadhi by vitiating doshas and dhatus.

Various factors are mentioned for the etiology of the disease. In the context of

Pandu roga all factors responsible for aggravation of pitta are termed as specific

nidanas. It can be stated that pitta prakopa nidanas cause the disease. The ahara and

vihara which are responsible for the disease can be divided into following types.

i. Ahara (Diet related factors)

ii. Vihara (behavior related factors)

iii. Manasika (psychological factors)

iv. Nidanardhakara Rogas (other diseases leading to Pandu) and

v. Acquired by papakarma (sinful act)

Ahara (Diet) related factors

1. Atikhara dravyas

2. Ati amala dravyas

3. Ati katu dravyas

4. Ati kashaya dravyas

5. Ati Ushana dravyas

6. Ati teekshana ahara

7. Vidagha dravyas

8. Asatmya dravyas

9. Nishpava

10. Masha

11. Pinyanaka

12. Tilataila

13. Mritbhakshanam (geophagia and pagophagia)

In the above stated factors kshara, amla, katu, lavana dravyas directly aggravate

to pitta. Especially, amlarasa does kapha vilayana, pitta vardhana, rakta dooshana and

sydhilya (increased catabolism). Ati lavana rasa intake leads to Raktapitta,

Amalapitta, Indralupta, vatarakata and other “pitta-rakta” related disorders.

Viruddhahara leads to vitiation of “tridoshas”. Masha is ushna veerya and in turm

increases pitta, Tila is pittakara and ushna veerya.

Ati teekshana ahara causes daha as it is of Agni boota predominance. Madhya

does pitta vitiation.

Vihara related factors:

1. Diwaswapna

2. Ati vyayama

3. Ati maidhuna

4. Panchakarma vaishamya

5. Nidra nasha

6. Vega dharana

7. Rutu Vaishamya

8. Rakta mokshana vaishamya

In the above mentioned factors ativyayama and ati mydhuna leads to increased

catabolism, thus contributing to the cause of the disease. Panchakarma vaishamya

vegavaroodha does vitiation especially to vata and thus cause disease pandu roga.

Among all Panchakarma vyshamyas, Atiraktasravam during rakta mokshana is also a

cause for the occurence of the disease.

Manasika factors:

1. Kama (desire)

2. Chinta (thinking)

3. Bhaya (fear)

4. Krodha (anger)

5. Shoka (sorrow)

Kama, shoka and bhyaya vitiate vata, krodha vitiates pitta, and chinta vitiates

vata kapha and produce vataja, pittaja and kaphaja predominant Panduroga.

Nidanardhakara factors: The disease which cause Pandu are grouped as

1. Rakta pradara

2. Raktapitta

3. Arshas

4. Krimiroga

5. Adhika raktasrava (due to abhighata)

6. Rakta arbuda

7. Rakta gulma

8. Pleehodara

9. Katikatarunamarma vedha

10. Yakrit pleeha vedha

11. Rakta atipravartanam

12. Hridroga

Apart from the above disease, all the conditions that end up in blood loss leads to

Pandu roga.

Papakarma factors: (Sinful act)

A person acquired Panduroga by sinful act according to the references from

Vaidya chintamani i.e. one who steals things of Gods and Brahmanas, one who does

not complete Agnistomadi karmas and one who kills a woman. Such persons acquire

Pandu with severe headache and with symptoms of kshaya. Such type of Pandu does

not get cured within nine years.

Thus the nidana of panu roga has been elaborately touched and discussed

because it has been said that "Chikitsa is Nidana Parivarjanam"Nidana as mentioned in different classics

Ahara (Diet) related factors:

S.No. Description Charaka Susrutha Madhavakara Haritha Vagbhta1 Kshara + - - + -

2 Lavana + + + + -

3 Katu - - - - +

4 Kashaya - - - + -

5 Atiteekshna - + + - -

6 Atiushna + - - - -

7 Virudha + - - - -

8 Vidagda + - - - -

9 Asatmya + - - - -

10 Nishpava + - - - -

11 Masha + - - - -

12 Pinyaka + - - - -

13 Tila taila + - - - -

14 Madya + - - - -

15 Mireya + + + + -

16 Amla + - - + -

17 Mrittika + + + + +

2. Vihara factors:

S.No. Description Charaka Susrutha Vagbhta Madhavakara Haritha

1 Diwaswapna + + + + +

2 Vyayama + - + + -

3 Maidhuna + + + - +

4 Panchakarma + - - - +

vaishmya

5 Rutuvaishamya + - - - -

6 Vegavidhrana + - - - -

7 Nidranashnam - - - - +

8 Avyayama - - - - +

9 Shrama - - - - +

3. Manasika factors

S.No. Description Charaka Susrutha Vagbhata Madhavakara Haritha

1 Kama + - - - -

2 Chinta + - - - +

3 Bhaya + - - - -

4 Krodha + - - - -

5 Shoka + - - - -

Charaka mentioned Pandu roga is the "Santharpanajanya Vyadhi". Though the

intake of food may be more, the disease is aquired due to pitta Vardhaka ahara as well

as viharas. This imbalanced diet contains more fats, however deficiency of vitamins

and minerals leads to anaemia.

ETIOLOGICAL FACTORS

Anaemia is caused due to various factors. They are grouped into following heading.

1. Idiopathic causes

2. Haemorrhagic anaemia

3. Dyshaemopoietic anaemia

4. Haemolytic

5. Aplastic or non-functioning Bone marrow

1. Idiopathic: Causes may be due to the anorexia. Psychiatric, autoimmune disease.

2. Haemmorhgic factors: Loss of blood due to trauma and various other causes.

a. Acute: Acute and massive haemorrhage in antipartum haemorrhage, post

partum haemorrhage, haematemesis, haemoptysis.

b. Chronic: Small and recurrent bleeding tendency such as piles, bleeding gums,

hookworms, etc, menorrhagia in females, chronic ulceration of gastro intestinal

tract, GIT malignancy, long standing haematuria oesophagical varices.

3. Dyshemopoietic (or) Due to defective blood formation:

a. Due to nutritional deficiency (or) deficiency of extrinsic factors

b. Failure of absorption of iron, proteins, B12, folic acid and vitamin C.

c. Lack of iron storage (due to liver damage large amount of iron & other

necessary elements are not stored and leads to anaemia).

d. Lack of releasing factors due to spleen enlargement.

e. Defiiency of certain minerals like copper, cobalt, manganese and certain

hormones like thyroxine, etc.

f. Endocrind disorders eg. Myxodema, Addisons disease.

4. Hemolytic anaemia:

Normally RBCs are destroyed by Reticulo – endothelial cells, situated in liver, spleen

and bone marrow.

a. Due to abnormal formation of RBCs as in spherocytosis, thalassemia and sickle

cell anaemia.

b. Due to circulating haemolytic agential haemolytic anaemia and paroxysmal

haemoglobinuria.

c. Incompatibility of blood groups and Rh incompatibilities.

d. Bacterial infections – septicemia

e. Chemical agents – Aspheramine, coaltar, derivatives and poisoning.

f. Snake venom and other poisionous bites cause anaemia due to haemolysis.

g. Cytotoxic drugs such as phenyl hydrazine, hydrochlorosis and quinine also

cause haemolysis.

5. A plastic (Non-functioning) bone marrow:

a. Lack of Utilization of haemopoetic factors by bone marrow is seen in primary

Aplasia.

b. Sometimes drugs such as chloromycetin, quinine, Benzol, Aspheramine and

gold salts depress the bone marrow, causing secondary Hypoplasia. Radium

salts, radioactive materials and X-rays also cause bone marrow.

Warm – infestation:

Parasites may cause disease Anaemia due to their presence in the lumen of the

intestine, due to infiltration into the blood stream.

Ex. Malarial Parasite may cause Anaemia due to Haemolysis (Distruction of Red

cells).

Nematodes like Ascaris, Enterobiasis (Pin warm), Tape warms and Hook warms

are caused to Anaemia in human being especially in children during the first decade of

life.

In effects individuals at all socio-economic level especially children crouded living

conditions predispose individuals to infection.

The larwas are found in warm, damp soil and infect humans by penetrating the skin.

They migrate to the lungs ascend thetrachea are swallowed and reside in the institine.

The warms then mature and attach to the intestinal wall, when they suck blood, and

shed eggs, caused by the Symptoms like Anorexia, Indigesation, Abdominal pain and

Fullness of abdomin, and Diarrhoea occurs. The major manifestation of infection is

subsequent Anaemia.

References:

Charaka Samhita, Chikista Sthana 16/7-11

Susrutha Samhita, Uttara Sthana 44/1-3

Astanga Sangraha, Nidana Sthana 13/3-6

Astanga Hridaya, Nidana Sthana 13/1-3

Madhavanidana 8/2

Hareeta Samhita, Triteeya sthana 8/3-5.

A text book of Human physiology by Dr. Sahana chakraborthy and Ghosh.

A text book of Pathology by Boiyd

Nelson Text Book of Paediatrics.

POORVA ROOPAAccording to susrutha, the sanchita and prakopita doshas are occumulated in a

particular stana it is termed as “Stana samshrayaavasta” a premonitory signs and

symptoms of manifestation of vyadhi. Those signs and symptoms which appears

earlier to the actual disease, as they are not clearly recongnisable and few in number.

These are called poorvaroopas, This is very important stage, which is to be observed

by the physician because it would be very easy to prevent the disease.

“Poorva roopam pragutpathi lakshanam Vyadhi”-

(Charaka Nidana – I Chapter)

Poorvaroopam is a state where the prodromal signs and symptoms of a disease

start to occur. In other words, it is described as the early stage of any disease. It is that

state of the disease, where Dosha – Dooshya Sammoorchana occurs, i.e. there begins

an interaction between the doshas and the dooshyas.

Poorva Roopa is of the following two types

1. Samanya poorva roopa

2. Visesha poorva roopa

Samanya poorva roopa gives information about the disease, which occur in the

following days but not the detailed description of the predominant dosha. Visesha

poorva roopa gives most of the details of the occurring disease at an early stage.

Samanya poorva roopa of Pandu are:

1. Twak sphotana

2. Shteevana

3. Gatrasaadana

4. Koota shodha

5. Avipaka

6. Hridaya spandana

7. Twak rushata

8. Swedabhava

9. Sharama

10. Shareera pandutwa

11. Mrit bhakshanaapeksha

12. Alpagni

13. Shareera krishatwa

14. Angasaada

15. Aruchi

16. Vit., Mootra, Peetatwam

Poorvaroopa – According to different acharyas:

Sl Poorvaroopa Charaka Susrutha Vagbhata Hareeta

1 Twaksphotana - + - -

2 Shteevana - + - -

3 Gatrasaada - + - -

4 Kootashodha - + - -

5 Avipaka - + - -

6 Hridayaspandana + - - -

7 Twakrushata + - - -

8 Swedabhava + - - -

9 Shrama + - - -

10 Shareerapandutwa - - - +

11 Aruchi - - + -

12 Vit, mootrapeetatwam - + - -

13 Mritbhakshanaapeksha - + - -

14 Alpagni - - + -

15 Angasaada - - + -

16 Shareerakrishatwa - - + -

Though there is no detailed description of the vishesha poorva roopas by any of

the classics, we can divide the above poorva roopas upon the doshic predominance

and can classify as follows:

S.No. Vataja P.R. Pittaja P.R. Kaphaja P.R. Mritbhakshana P.R.1 Twaksphotana Vit, mootra Shteevanam Mrit Bhakshana

Peetatwa Shteevanam

2 Angasada Avipaka Alpagni -

3 Gatrasaada - Aruchi -

4 Twakrushata - Hridayaspandana -

5 Swedabhava - Kootashodha -

6 Sareera krishatwa - Sareera pandutwa -

7 Shrama - -

POORVA ROOPA - MODERN ASPECT

There are no definitive prodromal symtpoms mentioned as such in case of

Anemia. Especially, these depend upon oxygen carrying capacity of the blood. The

severity of the signs and symptoms depend upon the degree of anemia, independent of

its type.

Lassitude and Fatigue, though are seen in the early stages of the disease, these

are seen in many other disease. Pallor of skin, mucous membranes, palms and

conjunctivae are seen after some period and these in addition to above may give a

better picture of this disease. The complete picture of the disease shall be discussed

under Roopa.

References:

Charaka Samhita Chikistasthana 16/12

Susrutha Samhita Uttara Sthana 44/5

Astanga Sangrata Nidanasthana 13/6

Astanga Hridaya Nidana Sthana 13/8

Hareeta Samhita, Trieeya sthana 8/6

Principles and Practice of Medicine by Davidson

ROOPAThis is the stage of a disease where the signs and symptoms of the disease are

totally manifested, this termed as fifth kriya. Kaala of ‘vyaktibhava’. When the

disease starts to take its stage forth kriyakala namely in the Stanasamshrayaavastha

or Poorvaroopavasta and when it is not treated the doshas get accumulated and

manifestiation into the diseased state – “ROOPA”.

“Tadeva vyaktatam yatam rupa mityabidiyate”

The poorva roopa which has attained vyakthavastha known as roopam. The

symtpems are mainly due to sroto dushti of the respective Srothases. The main srotas

involved in pandu roga is Rasavaha srota drushi.

Hence, almost all of Rasavaha sroto dushti lakshanas can be observed in pandu

symptomatology. These are Aruchi, Ashraddha, Agnimandya, Hrillasa, Arasagnatha,

Gouravam, Tandra, Angamarda, Pandutwam, Jwara, Klaibhyam, Sada, Krishnagata

and phalitya.

In general, the signs and symptoms of pandu roga are as follows:

1. Dhatu shaithilya 2., Alpa rakta 3. Ojoguna kshaya

4. Alpa medas 5. Sithil endriya 6. Hritdrava

7. Shoona akshi 8. Koota sadana 9. Kopana

10. Shteevana 11. Alpavak 12. Hataanala

13. Anna dwesha 14. Karna kshweda 15. Dourbalyata

16. Sisira dweshi 17. Shrama 18. Bhrama

19. Shoola 20. Jwara 21. Swasa

22. Gourava 23. Gatra peeda 24. Aruchi

25. Sheerna loma 26. Hata prabha 27. Nidradhikyata

28. Pindiko dwestta 29. Kati, Uru, Pada – ruk 30. Sannasakti

31. Sphurana 32. Nakha vakrata 33. Swetha akshi

34. Arosha naayasa

In addition to the above, kshayalakshanas of Rasa, Rakta, Medo, Mamsa, and

Ojus can also be observed in panduroga.

The disease is classified into five types, according to the involvement of doshas.

1. Vataja pandu roga

2. Pittaja pandu roga

3. Kaphaja pandu roga

4. Sannipathaja pandu roga

5. Mritbakshanajanya pandu roga

The lakshanas of all these varieties differ from each other, and they are stated in

below.

Lakshanas of vataja pandu roga:

S.No. Symptoms/sign Cha Su Va Ma Bha Ha

1 Aruna angata + - + + + -

2 Aruna nakha - - + - - -

3 Aruna netra - - + + + -

4 Aruna sira - - + + - -

5 Rkshna mala, mootra - - + + + -

6 Ruksha netra - - + - - -

7 Ruksha nakha - - + - - -

8 Ruksha anga + + + + + -

9 Krishna netra - + + + + -

10 Aruna mala mootra - - + - + -

11 Krishna nakha - + + - - -

12 Vata vikara - + - + + -

13 Anga marda + + - - - -

14 Jwara + - + - - -

15 Toda + - - - - -

16 Kampa + - + + + +

17 Parshwa shoola + - + + + -

18 Shirah shoola + - + - - -

19 Vitshoola + - + - - -

20 Asya vairassya + - + - - -

21 Shopha + - + - - -

22 Anaha + - + + + -

23 Balakshaya + - - - - -

24 Bhrama - - - + + -

25 Parushata - - - - - +

26 Sirogurava - - - - - +

27 Gadhavitakata - - - - - +

28 Ruksha sira - - + + - -

Lakshnas of pittaja pandu roga:

S.No. Symptoms/sign Cha Su Va Ma Bha Ha1 Shareera peeta + + + + + +2 Shareera Harita + - + - - -3 Peeta mala, mootra + + + + + +4 Peeta netra - + + + + -5 Peetha nakhata - + + - - -6 Peetha sira - + + - - -7 Harita sira + - + + + +8 Jwara + - + + + +9 Daha + + + + + +10 Trishna + - + - - -11 Moorcha + - + - - -12 Sweda + - + - - -13 Annadwesha + - + - - -14 Katu kasyam + - + - - -15 Amlodgara + - + - - -16 Ushna, Amla anupasayata + - - - - -17 Vidaha + - - - - -18 Dourgandha + - + - - -19 Binnavarchasa + + + + - +20 Dourbalya + - - - - +21 Pitta vikara - - - - - -22 Tama + + + - - -23 Shopha - + - - - +

Lakshanas of kaphaja pandu roga

S.No. Symptoms/sign Cha Su Va Ma Bha Ha

1 Swetha avabhasata + + + + + -

2 Sukla akshi + + + + + -

3 Shukla nakha - + + - - -

4 Shukla, mala, mootra + + + + + -

5 Shukla sira - + - - - -

6 Gouravam + - + + + +

7 Tandra + - + + + +

8 Chardi + - - - - -

9 Praseka + - + + + -

10 Lomaharsha + - + - - -

11 Angasadha + - - - - -

12 Moorcha + - - - - -

13 Bhrama, klama + - - - - -

14 Swasa + - + - - -

15 Kasa + - - - - +

16 Alasyam + - - + + +

17 Aruchi + - - - - -

18 Vak, Swaragraha + - - - - -

19 Katu kamata + - - - - -

20 Ushna kamata + - - - - -

21 Swayadu + - - + + +

22 Madhurasyata + - - - - -

23 Lavanakamata - - + - - -

24 Swara kshaya - - + - - -

25 Sleesma vikara - + - - - -

26 Swedana - + - - - -

The main differentiating features of vataja, pitaja & Kapha

S.No. Lakshanas of pandu Vataja Pittaja Kaphaja

1 Varna of vit, mootra Krishna Peeta Sukla

Nakha and Netra

2 Jwara Present Present Present

3 Shotha Present Absent Present

4 Kamitwa Absent Seeta Ushna./katu

5 Mukha ruchi Vairasya Katu Madhura

6 Moorcha Absent Present Present

7 Pureesha Little in quantity Bhinna Constipated

8 Varna Aruna Peetha/haritha Swetha

9 Bala Decreased Decreased

10 Other characterstics Rukshatwa Daha Gouravam

Angamardha Trishna Tandra

Krodha Swedana Chardi

Parushatwa Anannabhilasha Loma harsha

Siroruja Vidaha Sada

Dourgandha Bhrama

Klama

Swasa

Kasa

Alasya

Aruchi

Vakgraha

Swaragraha

Laskhanas of Sannipataja Pandu Roga:

Sannipatajapanduroga basically occur by the vitiation of all the three doshas (Vata,

pitta & Kapha), it possesses all the features of pandu that are mentioned under their

respective tables. However the clinical features shall differ as per the doshadhikyata.

Hareeta mentioned that sannipataja pandu has the following lakshanas in

addition to above.

Tandra Hrillasa Kshudarthata Kasa

Alasyam Shosha Moha Jwara

Swayathu Vitbhada Trishna Glani

Vamana Purushanayana

Madhava nidana added Arochaka and Haterndiya to above features.

Mrit Bhakshanajanya Panduroga:

The name Mritbhakshana janya pandu, as the name indicates, occurs due to

intake of Mrittika (mud/pica). This geophagia vitiates all the three doshas. But

depending upon the rasa of mud eaten, any of the three doshas vitiate, predominantly.

Mrit generally contain ruksha guna in predominance. This makes the food

consumed and the srotas, to dry. This leads to obstruction of srotas and even vitiates

rasa and raktadi dhatus. So the following clinical features occur in pandu Roga.

1. Destruction of bala, varna and agni

2. Shotha of ganda, akshikoota, bhru, paada, nabhi and mehana

3. Krimikoshta

4. Kapha, rakta sahita pureesha

5. Atisara

6. Indriya dourabalya

7. Srotodusti lakshanas

8. Destruction of tejus, veerya and ojus, these are specific lakshanas in addition to

the specific doshas involved.

Modern aspectClinical Aspects of Anaemia

Clinical features of anaemia reflect the diminished oxygen carrying capacity of

the blood. Their severity depends on the degree of anaemia and the pace of its

development. The Signs and Symptoms are listed below.

S.No Symptoms Signs

1 Lassitude Pallor of skin, mucous, membrane2 Easy Fatigability Palm of hands, conjunctiva3 Palpitation Tachycardia4 Breathlessness on exertion Dyspnoea on exertion5 Dizziness Tachypnoea6 Throbbing in head & ears Palpitation8 Headache Cardiac dilatation9 Dimness of vision Systolic flow murmurs10 Insomnia Oedema11 Angina Platynychia12 Parasthesia of fingers Oedema of the feet

and toes13 Loss of weight Early graying hair14 Loss of appetite Glossities15 Diarrhoea Angular stomatitis16 Flatulence Smoothening of tongue17 Constipation Dyshphagia18 Low fever Rapid pulse19 Lack of concentration Signs of cardiac failure20 Backache Vagorous arterial pulsation21 Giddiness22 Faiting of spells of blackout23 Noises in the ears24 Urinary frequency nocturia25 Loss of libido and potency26 Menorragia27 Thin lusterless hair28 Amenorrhoea29 Delayed Purberty30 PICA

Though the person is anemia, one cannot find all the signs and symptoms

mentioned above since anaemia is caused by different etiological factors, their clinical

features shall also surely differ.

Though the above mentioned clinical features give a clear idea of the disease,

diagnostic methods confirm the disease and aid in detection of the cause in many

instances.

INVESTIGATIONS

Blood examinations

1. Estimation of hemoglobin

2. Total RBC count

3. Total WBC count

4. Differential count

5. Packed cell volume (Hematocrit)

6 Blood picture

7. Electrophoretic pattern of hemoglobin

8. Erythrocyte sedimentation rate

9. Total plate let count

10. Plasma transferin

11. Total iron binding capacity

12. Serum ferritin13. Serum vit B12 levels

14. Serum folic acid estimation

15. Plasma LDH (Lactate dehydrogenase)

16. Lipid profile

17. Total bilurubin – Direct and indirect

18. Glucose profile

19. Serum proteins.

2. Urine examination: Urine must be examined for microhematuria, Albumin,

urobilurubin (bile salts and bile pigments), sugur and others.

3. Faeces: Faeces must be examined thoroughly for ova and cysts and for excessive

urobilurubin for occult blood and melena.

4. Bone marrow bipsy

5. E.C.G.: ECG should also be done because, most of the signs overlap with

congestive cardiac failure and other valvular heart diseases.

6. Endoscopy: sigmoidoscopy / proctoscopy / Gastroduodenoscopy

7. IVP : Intravenous pylogram may be useful in haematuria is present.

8. Jejunal biopsy

9. Cr-51 labelled RBC infiltration.

IRON DEFICIENCY ANEMIAS

Age Group: This type of anemia is mostly seen in children between ages of 6 months

and 2 years, and from 11 to 16 years due to spurts of growth during these periods.

This is also common in adult menstruating and childbearing aged females.

SEX: Iron deficiency anemias are mostly seen in adult females in their menstrual age

and it is almost universal during pregnancy.

DIETARY HABITS: Vegetarians are more commonly affected with Iron Deficiency

anemias than non vegetarians. Consuption of white bread, polished white rice, white

sugar etc. increases the disease incidence.

SOCIAL STATUS: Poor are predominantly affected than the rich.

CLINICAL FEATURES:

Due to Anemia: Insidious onset of easy fatigability, weakness, headache, body ache,

inability to concentrate, giddiness, palpitation, exertional dysphoea, anginal pain and

Hemic murmur.

a. Manifestation of underlying condition: For example, pain of peptic ulcer,

epigastric lump in carcinoma stomach

b. Due to Iron Deficiency Anemia

1. Tongue - Smooth and Pale (bald tongue) and Angular Stomatitis

2. Dysphagia - Formation of Mucosal webs (Plummer-Vinson Syndrome)

3. Gastritis

4. Nail changes - Thin and Fragile nails - Platynychia and Koilonychia

5. Hepatospleenomegaly

6. Pica - Perversion of appetite in form of Geophagia or Pagophagia

(excessive eating of rice)

7. Miscellaneous: Edema of feet, impaired renal function or

Hypoproteinemia, Amenorrhoea and Menorrhagia, increased intracranial

tension, long standing anemia leading to Fronto-Parietal eminence,

Parotid gland swelling and hair loss.

LABORATORY FINDINGS:

A. To establish & assess severity of anemia:

1. Blood Picture - RBC count, Hb%, and Hematocrit are decreased. MCV,

MCH, and MCHC are decreased.

2. Bone marrow - Increased cellularity from increased hemopoietic activity.

Bone Marrow Iron Stores are markedly decreased or absent.

3. RBC survival is decreased.

4. Serum Iron and Transferrin saturation are decreased. Iron Binding Capacity is

increased. Plasma Iron Clearance, Erythrocyte Iron turnover are increased.

5. Blood Picture- RBC count, Hb%, and Hematocrit are decreased. MCV, MCH

and MCHC are decreased.

6. Bone marrow - Increased cellurarity from increased hemopoietic activity

Bone marrow Iron Stores are markedly decreased or absent

7. RBC survival is decreased

8. Serum Iron and Transferrin saturation are decreased. Iron Binding Capacity is

increased.

9. Plasma Iron Clearance, Erythrocyte Iron Turnover are increased.

B. To determine cause of anemia:

1. Stool Examination for occult blood, bulky fatty stools, ankylostoma.

whipworm and amoebiea.

2. X-rays - barium meal and small bowel exam.

3. Endoscopy - Proctoscopy for detection of piles, Sigmoidoscopy and

Gastroduodenoscopy may reveal lesions not shown by x-rays.

4. Jejunal biopsy

5. Cr-51 labeled RBC injection shall detect loss of blood in faeces that detect GI

blood loss.

6. IV Pyelography

7. IV Pyelography

8. Selective angiography: If there is significant blood loss and no lesion has been

detected, local angimatous malformation.

MEGALOBLASTIC ANEMIAS

Megaloblastic anemia is caused by Vit. B12 Deficiency, folic acid deficiency,

and defective DNA synthesis (other than B12 and folic acid deficiences)

Clinical feaatures:

1. Due to anemia: Shortness of breath, dyspnoea, pallor and in older patients

angina or cardiac failure.

2. Gastrointestinal: Diarrhea, loss of appetite and weight and slightly yellow tint

of mucous membranes due to intramedullary breakdown of Hb & reduced

RBC life span.

3. Fever of mild degree

4. Mild Spleenomegaly only in 50% of patients

5. Neurological manifestation:

a. Neuropathy-Paraesthesia, stamping gait & positive Romberg's sign.

b. Subacute degeneration leading to increased leg reflexes & extensor

plantar response and sensory loss.

c. Optic neuropathy

d. Depression, impaired memory, and organic dementia

6. Miscellaneous features: Purpura & thombocytopenia, mild mal absorption

syndrome, sterility and wide spread skin pigmentation

Age: All age groups especially aged and elderly people.

SEX: Females of reproductive age are more prone for Megalobastic anemia and

during pregnancy this deficiency can even lead to umbilical cord and neural canal

deficits.

Dietary habits: Strict vegetarians (Veganism).

Social Status: Poor people are more sufferers of anemia

The above said Iron Deficiency anemia and megaloblastic anemias if untreated

lead to fatal Pernicious Anemia from severe form of blood disease, marked by

progressive decrease in RBC, muscular wekness, GI & neural disturbances

Age - 40 to 60 years

Sex - More in females

Race - Incidence highest in north Europeans

Family History - The disease is about 20 times more common in close relatives.

References:

1. Charaka Samhita, Chikitsa Sthana, 16th chapter

2. Susruta Samhita, Uttara Sthana, 44th chapter

3. Astanga Sangraha, Nidana Sthana, 13th chapter

4. Astanga Hridaya, Nidana Sthana, 13th chapter.

5. Madhava Nidana, 8th chapter

6. Hareeta Samhita, Tritiya Sthana, 8th chapter

7. Kashyapa Samhita, Sutra Sthana, 25th chapter

8. Davidsons Principles and Practice of Medicine

9. Current Medical Diagnosis and Treatment

10. Medicine for students by Dr. Golwalla

11. A.P.I. Text book of Medicine.

SAMPRAPTISamprapti is the stage wise manifestation of the disease. The disease process is

starts with nidana and then passes through Sanchaya, prakopa, prasara,

Stanasamsraya and Finally manifestation of Vyaktavastha, i.e. manifestation of

pandu. This complete disease process is called as samprapti. In other words

Samprapti gives detail information about the pathogenesis of the disease.

The term samprapti in madhavanidana is as below

"Yatha dushtena doshena yatha chanu visarpatu

Nivrutti Ramaya - Syasan samprapti jati ragati"

Samprapti can also be called dosha doosya sammurchanavasta of a particular

vyadi.

In pandu roga generally three dosas are involved and in particularly pittadosha.

The pitta prakopakara ahara and vihara are the causative factors of pandu. Because of

these nidnans pittavridhi takes place. Physiologically the formation of acchapitta,

occurs in Grahani during ahara parinama. But due to katu, amla, lavana, ushna ahara

and other causes mentioned earlier, vitiation of pitta takes place. Since Pachaka pitta

is situated in Grahani, the vitiated pitta affects the Agni. The drawatwa in this

vidagdha pitta reduces its teekshanatwa. This agni cannot digest the ahara consumed,

there by leading to vidagdha bhava.

Generally, after pachana, the food consumed is divided into Sarabhaga and

Kittabha by samana vayu and the saarabhaga is taken to hridaya. But due to vidagdha

pitta, pachana does not occur properly leading to dooshita annarasa. The annarasa is

taken by samanavayu to hridaya and transforms it into rasadhatu. The viharas like

vyayama, vyavaya etc cause vitiation of vyanavayu. The viitiated vyana vayu along

with pitta - dooshita rasadhatu circulates throughout the body through dasa dhamanis

that emerge from hridaya. The pitta dooshita rasa dhatu flows into the next dhatu for

its nourishment malformed rasa dhatu due to pittavidagdata, destructs the

raktadhatu poshakamsas and attains pandu roga, which will not be in a position to

nurish dhatus.

Finally rasadhatu lodges in the space between twak and mamsa. Then by

vitiating the kapha, vata, rakta, twak, and mamsa, it produces pandu, haritha and

haridra varnas, or various other discoloration of the skin. Of these colours, pandu is

seen predominantly. The formation of all the other dhatus is also impaired. As a

results of this, the formation of next dhatu i.e. raktadhatu is effected both qualitatively

and quantitatively. Even the essence which comes out from each dhatu also reduces in

its quantity. As the essence of all dhatus is ojus, its kshaya lakshanas can also be

observed on progression of the diseases.

In pandu the rasa dhatu dushti and there by its kshaya takes place. Hence in the

first stage of the disease, rasadhatu kshaya lakshanas are predominantly seen. Those

are Hritpeeda, Kampa, Shoonata, Trishna, Shabda Asahishnuta, and Swalpa cheshta.

In the later stages the kshaya lakshanas of other dhatus is also seen.

The nidanas for pandu pertaining to ahara are ati amla, atilavana, Atiteekshna,

madhy and mritsevana and diwaswapna and vitiation of rakta as well as ranjaka pitta.

As the place of ranjaka pitta and rakta vaha srothasas is yakrut and pleeha. The

nidanas which vitiate ranjaka pitta and rakta directly causes the kshaya of these two

and / or the qualities of these two are also altered. These are responsible for the

disease pandu. Hence ranjaka pitta and rakta kshaya lakshanas are observed in the

disease.

The consumption of mrit also vitiates the doshas and causes the disease.

Kashyarasa mrit vitiates vata, katu rasa mrit vitiates pitta and kapha is vitiated by the

madhura rasa mrit.

Generally mrit contains ruksha guna. Hence the consumption of mrit mainly

vitiates vata. Mrit does not contain any dhatu poshka amshas. It obstructs all the

srothasas as it does not get digested and prents the rasadhatu to enter into the other

dhatus. This impairs the formation of dhatus starting from rasa to sukra. This

impairs even the formation of ojus also. The resultant manifestations are loss of

energy of indriyas and tejus. Finally the disease sets in with bala, varna, and

agninashana, swelling of akshi, ganda, akshikoota, pada, nabhi, medra, krimikosta,

and atisara - as well as kapha - rakta yukta pureesha occurs. Thus samprapti of pandu

roga is discussed in detail.

References:

1. Charaka Samhita chikitsastana 16/6-11

2. Susrutha samhita nidana sthana,

3. Susrutha samhita, sareerastana

4. Susrutha samhita, uttara sthana 44/3

5. Ashtanga sangraha, sutra stana

6. Asthanga sangraha, Nidana stana 13/3-6

7. Ashtang Hridaya, sutrastana

8. Ashtang Hridaya chikitsastana 13/3-6

9. Madhava Nidana.

SADYA AND ASADYA LAKSHANASIt is very essential to decide the sadhya and asadhya of any disease before

attempting to treat it. As a general rule, the disease without any upadravas, or arista

lakshanas, which is newly manifested, which has less number of lakshanas and in

which only one dosha is involved is said sukhasadhya. Asadhya denotes the bad

prognosis of the disease. Asadhaya lakshanas are two types – Yapya and

Pratyakhyeya. Yapya is the term used when the disease is incurable and the patient

survives due to Ayusesha and the patient should have life long treatment.

Pratyakhyeya indicates achikitsa avastha of the disease.

If the patient acquired all the said lakshanas of the disease, and if it is of

chronic in nature, the disease is said to be pratyakhyeya. It has been mentioned that

the physician should leave the patient untreated, if the below mentioned asadhya

lakshanas are seen in the patient.

The following are the asadhya lakshanas of pandu

“Chirotpanna kharibhoota”1

1. Doshas occumulation in a large scale.

“Kalaprakarsha shoonana peeta darshee,”2

2. The patient has developed oedema and seeing all objects in yellow colour

“Sa kapha yuktha haritha varna baddalpa atisaree”3

3. When the patient passes baddha, alpa and haritha pureesha with kapha

“Asrikshaya swetangee”4

4. The patient is rakta kshaya – panduvarna sareera

“Chardi, moorcha, trishnardita deena swetati digdhangata”5

5. Pandu roga associated with chardi, moorcha, thrishna, deena and atipandu

varnam.

“Anta pradesha shoda and madhy sareera krisha”6

Shota in extremities and krishata in Madhya sareera.

6. When the patient is afflicted with sodha of the extremities with an

emaciation of the Madhya sareera.

Shota in guda, sephasa and mushka pradesha7.

7. When the patient has sodha of guda, shepha, mushka.

“Jwara, Atisara peedita pandu roga.”8

8. Pandu roga associated with jwara and atisara.

9. If the pandu rogi has massive intestinal worm infestation and pass feces with

blood and mucous.

10. Pandu rogi with swedana, dehajaadya, Swayadhu, Vamana, Nyanga, Sosha,

Kasa, Nidra and Brama.

The knowledge of sadhy asadhyata is essential to include or exclude the patients

in the study. If the patient develops the above clinical features, then the physician

should leave the patient untreated.

References:

1. Charaka chikitsa stana 16/32, 36

2. Susrutha uttara sthana 44-40

3. Astanga hridaya Nidana 13/15,16

4. Bhava prakasha madhyama kanda – P Prakaranam / 13,14,15,17

5. Vangaseena 19, 15

6. Yogaratnakaram 13, 16

7. Susruta sutra stana 33/22

UPADRAVAS AND ARISHTA LAKSHNAS

Upadravas: Any vyadhi or clinical features appearing on the later stage of a main

disease due to improper management are called as upadravas of the disease. When

upadravas occurred the disease becomes very difficult to treat. It denotes that the

disease should be treated as early as possible before appearing upadravas.

The upadravas that are associated with Pandu roga are as follows:

1. Aruchi 2. Pipasa 3. Chardi

4. Jwara 5. Shirashoola 6. Agni mandyam

7. Kanta shopha 8. Daurbalyam 9. Moorcha

10. Klama 11. Hridaya peedana 12. Swasa

13. Atisara 14. Kasa 15. Shoola

16. Daha 17. Ajeerna 18. Swarabedha

19. Shotha 20. Swarasada

Hence Pandu should be treated as early as possible before upadravas appear. The

dosha involvement in the upadravas may be equivalent to the main disease (or) may

not be.

Arishta lakshanas:

Arista lakshanas are Asanna marana lakshanas. These are the clinical features that

appear in the patient when the prognosis is very worse and the patient is nearing death.

In other words the signs & symptoms, which indicate death, are the Arista lakshanas.

The arishta lakshanas that appear in Pandu roga are given below:

1. Pandu varna danta, nakha netra and twak

2. Shopha and swasa

3. Trishna yukta shoola.

4. The patient expires if he gets the dream of eating pale coloured food

5. Pandu rogi sees that the environment in pandu varna.

6. Pandurogi dies immediately when pandu is associated with prameha and

bleeding through nostrils

As these above Arishta lakshanas point out the worst out come. A wise physician

should not treat them.

References:

1. Susrutha uttara stana – 44/13,39

2. Susrutha sutra shtana 33/22, 29/69

3. Hareetha samhit 4/37, 4/24

4. Susrutha sutra stana – 29/69

5. Bhavaprakasha madhyama kanda 16

6. Vanga sena 26/15

7. Yogaratnakara - /15

CHIKITSA KRAMAThe chikistsa karma means. Stage – wise treatment program of the disease. In

general, the three principles of treatment mentioned in ayurveda are

Diavavyapasraya, Yuktivyapassraya, and Satwavajaya. Daivavyaaprasraya

chikista mainly depends on praying God, doing yagnas and yagas, doing good deeds

etc Yuktivyapasraya chikitsa of pandu roga includes the following principles.

1. Nidana parivarjana

2. Snehana chikitsa

3. Shodhana chikitsa

4. Samana chikitsa

1. Nidana parivarjana:

“Samkshepathaha kriyayogo nidana parivarjanam”

Nidanaparivarjana is the first and fore most line of treatement for any disease.

The nidana (causative factors) mentioned earlier are to be avoided.

The nidana karanas of pandu roga are katu, amla, Lavana, Ushna, Teekshna

aharas, viharas – Vyayama, Vyavaya, Manasika karanas are Kama, Krodha, Bhaya,

Chinta, Shoka etc. karanas (causative factors) of pandu should be avoided.

2. Snehanam chikitsa:

Sadyanta pandvamaynam samekhaya snigdham ghritenordva madascha suddam.

Sampadayet kshaudra ghrita pragadair haritaki churnayutai prayogai

Snehana and swedana chikitsas are the poorva karmas of shodana chikitsa, but

swedana chikitsa is contra indicated in case of pandu roga, because it is pitta

pradhanavyadhi. The patients of pandu have dhatu kshayam which is due to improper

nourishment of rasadi dhatus. As a result, rukshatwa occurs in the body. This is a

necessary treatment before any shodhana karma. Shehana does srotho mardhava and

helps the doshas come out freely when sodhana karma is done. Snehapana is even

more important in case of mrit bhakshana janya pandu, because the mrit causes

rukshatwa in the srothas and causes obstruction in srotas. Sneha karma is indicated

before and after shodhana chikitsa in Mrit bhakshana janya pandu. Since Pandu

roga is pitta pradhana disease, the following tiktaghritas are mentioned for sneha

karma.

1. Pancha gavya ghritam

2. Maha tiktaka ghritam

3. Kalyana ghritam

4. Dadimadi ghritam

5. Katu ka rohinyadhi ghritam

6. Pathya ghritam

7. Danthi ghritam

8. Haridradi ghritam

9. Triphala ghritam

10. Draksha ghritam

11. Tilvakadi ghrita

12. Brahatyadi ghritam

3. Shodhana karma:

Charaka, Vagbhata and others recommended strong emesis and purgation after

giving oleation therapy.

Shodhana karma pulls out the doshas with their roots and prevents the

reoccurrence of the disease. The shodhanakarma indicated in pandu are Urdhwa

shodhanam (Vamana) and Adhah shodhanam (verechana)

A) Urdhwa shodhanam (vamana): Charaka stated that teekshana guna yukta

vamana oushadhas are indicated in pandu roga. Though susrutha contraindicated

vamana in pandu roga. Dalhana advocated Mridu vamana, when Rutu, Desha, Kala

are in favour. The drugs that are mentioned for vamana karma are

1. Dhamargava

2. Ikshwakum

3. Kritavedana.

B) Adhah shodana (virechana): Virechana is indicated in all types of pandu.

Hareetaki is advocated for virechana along with the following drugs.

1. Gomootrayukta dugdam

2. Dantiphala rasa and draksha choornam

3. Aragwadha majja with trikatu choornam

4. Phala ghrita

5. Tilwaka ghrita

6. Dadimadya ghrita

7. Pathyadi ghrita

8. Haridra di ghrita

9. Danti ghrita

10. Drakshadi ghrita

11. Doorva ghrita.Drugs for shodhana karma in panduroga according to doshic predominance :(Hetuviparitardakari chikitsa):

Name Vataja Pittaja Kaphaja Tridoshaja Mritbhakshanajanya

Cha Snigdha Tikta and Katu ruksha Tridoshahara Strong samshodana

& Madhu sheeta and Ushna of GIT

Su Snigdha Tikta and Katu ruksha Tridoshahara -

& Madhu sheeta and ushna

Vag Durgs Drugs of More Tridoshahara Strong purification

Possing bitter taste pungent dry therapy

sneha and cold and hot

potensive potency

BR Medicines Tikta and Katu ruksha Tridoshahara Strong purification

with gruta sheeta and ushna therapy

base medicines medicines

BV Mediciens Tikta and Katu ruksha,Tridoshahara Strong purification

with gruta sheeta and ushna therapy

base medicines medicines

YR Medicine Tikta and Katu ruksha, Tridoshahara Strong purification

with gruta sheeta and ushna therapy

base medicine medicines

4) Shamana chikitsa:

Samana karma of pandu according to doshic predominance

“Vatheke sneha bhuyestam paitthike tikta sheetalamSlaishmike katu tiktoshnam nimishramam saannipatheki”

l Vataja pandu roga is to be treated with snigdha and madhura dravyas.

l Pittaja pandu roga is to be treated with Tikta and Seeta dravyas.

l Kaphaja pandu roga is to be treated with katu Tikta rasa, and Ushna gunadravyas.

l Sannipathaja pandugaroga is to be treated with mishrita dravyas.

In shamana chikitsa, the following drugs are mentioned:

Single drugs:

Herbal drugs Mineral drugs

Pathy Loha bhasma / choorna

Amalaki Mandoora bhasma

Yashtimadhu Kaseesa bhasma

Draksha Abhraka bhasma

Brihat panchamoolas Swarna maksheka bhasma

Guda Silajit

Tila Pravala bhasma

Haridra Mukta bhasma

Shunti Sankha bhasma

Pippali Jasada bhasma

Bhringaraja Kantha bhasma

Kumari Tamra bhasma

Punarnava

Compound Herbo – Mineral preparations

1. Navayasa churna (Cha.Chi.16)

2. Yogarajam (Cha.Chi.16)

3. Mandhura vataka (Cha.Chi.16)

4. Ayoraja churnum (Cha.Chi.16)

5. Punarnava manduram (Cha.Chi.16)

6. Goudarista (Cha.Chi.16)

7. Beeja kalista (Cha.Chi.16)

8. Shilajet vataka (Cha.Chi.16)

9. Vyoshadhi choorna (As.Hri)

10. Kantavallabha ras (B.R.)

11. Hamsa mandooram (Y.R.)

12. Trilokyanath ras (Y.R.)

13. Chandra suryathmaka ras (Y.R.)

14. Prana vallabha ras (Y.R.)

15. Panchananavati (B.Ratna)

16. Anandodaya ras (B.Ratna)

17. Trilokya sundara ras (V.Chi)

18. Trimurthi sidda ras (V. Chi)

19. Rasa sindhoora bhooshana ras (V.Chi)

20. Udaya bhaskara ras ((V.Chi.)

21. Kameswar ras (V.Chi)

22. Pandu sudana ras (V.Chi)

23. Vangeswar ras (V.Chi)

24. Loha sundara ras (V.Chi)

25. Siddha mandoora (V.Chi)

26. Bala suryodaya ras

27. Kanta vallabha ras

28. Rajatha loha rasayanam

29. Sodhari mandoora

Avalehyas

1. Datri avalehya

2. Mandooradi avalehya

3. Vidangadi avalehya

4. Chinchadi Lehya

5. Chawan prashavalehya

Asava / Arishtas

1. Goudarishta

2. Beejakarishta

3. Dhatryarishta

4. Lohasava

5. Ayaskriti

6. Bringarajasavam

7. Kumari asavam

8. Punarnavasavam

Anupaana:

The substance that is consumed along with or after the intake of oushadha dravya is

Anupana. This may be either solid or liquid in nature. Anupaana should fulfill the

following principles.

1. It is pacify the atiteeskha guna, vyavayi and vikasi gunas of the main drug e.g.

Ghrita, Takra and Ksheera.

2. It is to stimulate the action if the drug is less potent. E.g.: Trikatu and gomootra

3. To carry the drug to specific location where its action is needed. For this a

dravya possessing yogavahi guna is needed. Eg. Madhu.

4. A drava dravya is needed as an anupana for easy swallowing of choorna (or)

gutika.

5. To create the palatability if the drug cannot be swallowed because of

reluctance.

The following are a few anupaanas mentioned in the context of pandu roga by various

authors.

1. Takra

2. Godugdha

3. Goghrita

4. Jala

5. Ikshurasa

6. Madhu

7. Gomootra

8. Triphala kashaya

9. Buffalo’s milk / mootra

Susruta mentioned that if a person had profuse blood loss he should drink blood

with madhu or take liver of a goat. (Su.Utt 44).

References:

1. Cha. Samhita chi. 16th chapter

2. Susruta, uttara, 44th chapter

3. Asthanga sangraha. Chikitsa 18th chapter

4. Ashtanga Hridaya chikitsa 13th chapter

5. Basava rajeeyam

6. Yogarathnakara

7. Bhaishajya Ratnavali

8. Vyadhya chintamani

9. Vydhya yoga Ratnavali

10. Sahasra yoga

11. Gada nighantu

12. Ayurveda vignanam

13. Saranga dhara samhit

PATHYA AND APATHYASThe knowledge of Pathya and Apathya is essential in treating the disease. All

the nidanas mentioned in nidana aspect are to be strictly considered as apathyas and

are to be avoided.

Those aharas and viharas, which are against the nidana as well as the disease are

called ‘Pathyas’. In contrary, the aggregating factors of the disease are called

‘Apathyas’.

Pathya (Upasaya): Food that are capable of causing agnideepana should form as

important principles of pathya – vyastha of pandu roga.

1. Rasa: Madhura, tikta, kashaya rasa

2. Guna: Guru, Rukshana, Teekshna gunas

3. Panchakarma: Vamana & Virechana

4. Ahara: Ahara – Godhuma, yava, shashtika danya, salidhanya

5. Yusha: Mamsarasa – Jangala mamsa & shringifish

7. Vegetables: Patola, vrudha kooshmanda, tarunakadhali phala, bimbi, vartaki,

lasuna dwaya and Jeevanthi

8. Others: Guduchi, Tanduleeyajalam, Punarnava, dronapushpi, Hareetaki,

Amlaki, Butter milk, Payasa, Ghee, Sowvearaka, Tushodaka, Navaneeta,

Gandha sara, Haridra, Vasa, Dadima, Nagakesara yavakshara, Lohabhsma and

Kunkuma.

9. Fruits: Draksha, karjura, and mango fruits

Apathyas:

1. Guru: Guru, ruksha, teekshana gunas

2. Rasa: Katu, amla rasa

1. Panchakarma: Raktamokshana, Dhumapana & Swedana.

2. Vihara: Atimaidhuna

3. Mamsarasa: Gramya mamsa rasa

4. Others: Shimbi, chitraka, masha, ambupana, pinyaka, tambula, sarsapa, sura,

all kinds of amla and virudha ahara.

Even the nidanas mentioned for the disease can also be considered as apathyas.

The knowledge of pathya and apathya is essential in diagnosing the disease. When the

nidanas, poorva roopa and roopa are not giving the perfect knowledge of the disease.

References:

1) Susruta samhita, Uttara Sthana, 44th chapter.

2) Hereeta samhita, Triteeya Sthana, 8th chapter

3) Basavarajeeyam Panchama Prakaranam

4) Asthanga Sangraha, Chikitsa Sthana, 18th chapter

5) Yogaratnakara, Madhyama Khanda.

CRITERIA FOR SELECTION OF THE DRUGThe drug selected for present clinical study is "Bhaskara Lavana Churnam". Its

anupana is "TAKRA". The administration of Bhaskara Lavana Churnam is advised in

the condition of panduroga. The drug has been selected to evaluate its efficacy in

pandu roga. The reference to the present clinical study is taken from the Baishajya

ratnavali.

"Pleehanamasmari Chaiva Swasakasaodara krimeen

Visheshatah Sarkaraadeen rogaannanavidhamstha the

Pandurogamseha vividhannasayatyasanirya tha"

(Bhaishajya ratnavali-Agnimandhya chiktsa)

The administration of Bhaskara lavana churna is advised in the condition of

Pandu, Pleehavyadhi, Krimi, Ajeerna, Aruchi, Arshas, Shoda, Amadosa. The drug has

been selected to evaluate its efficacy in pandu.

The preparation is non contraversial and the ingredients are easily available. This

formulation is easy to prepare and free from toxic effect.

The compound herbo mineral drug Bhaskara lavana churnam consists of

ingredients Samudra lavana, savarcha lavana, saindava lavana, Bida lavana, Dadima

beeja, Pippali, Pippalimula, Dhanyaka, Kalajeera, Teja patra, Talisa patra,

Nagakesara, Amla vetasa, Kalimareecha, Swetha jeera, Sunti, Twak, Ela. So this

Bhaskara lavana churnam mainly Tridoshahara, rasayana, Deepana, Pachana, Hridya,

Balya, Ruchya properties. It helps in pitta dosha samana, Deepaneeya and rakta

vardhaka. It has the direct action on Amasaya, Yakrit and Ranjaka pitta.

Agni vikriti is another importent clinical condition of pandu roga. Samagni is an

essential factor for the proper digestion and assimilation of ahara rasa, with the

mandagni avastha samyak ahara rasa formation will not take place. According to

charaka rakta poshakamsas are present in rasadhatu and owing to improper rasa

formation, proper development of raktadhatu is not possible, and the above condition

results in raktalpata.

In Bhaskara lavana choorna the pippali, pipplimula, tejo patra, Amla vethasa,

Jeeraka, Sunti, Twak and Ela mainly possess the properties of pitta dosha shamana

Agni Deepana, pachana and raktavardhakas, therefore helps in the production of

intrinsic factor and assimilation of extrinsic factor. It also avoid the accumulation by

virtue of its purgation property.

The pandu roga is pitta prakopaka vyadhi. In general the salts, main the saindava

lavana being seetagunam, Snigdhaguna, Avidhahi, Madura vipaka and Tridoshahara.

It acts pitta samaka. All salts are accepted as good preservatives which help in

reataining the potency of the prepared medicine for longer periods.

The pippali is explained as Rasayana in Ayurveda, addition of pippalli and

lavana churnas to the ingredients may help in faster absorption of the drug.

The Dadima, pippali, pappli mula, Dhanyaka, jeeraka, Tejo pathra and Twak

contains the property of krimigna. So are responsible for the elimination of worm

infestation, which is the one of the cause of the pandu roga.

The pippali, Amlavetasa, Twak, Talesaptra and contains the property of

"Ruchyam". In pandu roga imparment of the taste was seen due to rasa and Rakta

dhatu dusti. So this may help to increase the taste.

The Shunti, Jeeraka, Dhanyaka, contains 'grahi' guna, that is responsible for the

active absorption of lohasma in ahara and oushadha.

The Balya property of swethajeeraka assists in alleviating the dhatukshya and

ojokshaya, present in Pandu Roga.

The statement "Samanyam Ekatwa karam" mentioned in ayurvedic classics is

justified by asrik prasadana propperty of Dadima, Shunti, Jeeraka in pandu roga.

One of the sign of anaemia i.e. Palpitation is relived by the Hridya property of the

Amlavetasa, Dadima and Shunti.

DESCRIPTION OF INDIVIDUAL DRUGS

SAINDHAVA LAVANA

Synonyms: Sitasiva, manimantha, and sindhija, (Saindhara, sindhuphala, vasira,

sindhudesaja, Sindhu mandaja, sivasidda, palga)

Telugu - Saindava lavanam

Hindi - Saindha namak

English - Sodium chloride

Rasa - Lavana, Madhura

Guna Laghu, snigha, sukshma

Veerya - Seetha

Karma - Ruchyam, Agnideepanam, Amapachanam, Vrushyam,

Netryam.

This is commonly known as Rock-salt and is obtained in the form of hard lumps

in the mines in Beluchistan, sindh and upper Punjab. It is natural sodium-potassium

chloride.

SAMUDRA LAVANA

Rasa - Tikta, madhura

Guna - Guru

Veerya - Not very hot

Vipaka - Madhura

Karma - Agnideepanam, Virechanam, Ksharam, Not vidhahakaram(Slight alkaline), Shleshmakaram, vataharam, not causing

dryness, not causing coldness.

This is commonly salt prepared by evaporating sea water and is sodium

chloride in impure form.

SAUVARCALA LAVANASynonyms: Sauvarcala, Rucaka, Manthapaka

Telugu - Sauvarchala lavanam

Hindi - Kalanon

English - Black salt

Guna - Laghu, Visha, Sukshma,

Karma - Ruchyam, Bhedanam, Agnidepanam, Amapachanam, Slight

snehanam, Vataharam, not causing great increasing

Pitta, Vishadam, Udgara shuddi, Vibanda, Anaha, Shoolaharam.

BIDA LAVANAM

Synonyms - Bida Lavana, pakya, krtaka, dravida and asura

Telugu - Bidalavanam

Hindi - Viriya, Kalanamak

English - Black salt

Guna - Laghu, Tikshna ushna, ruksha, vyavayee

Veerya - Ushna

Karma - Slightly alkaline, Vata kapha Haram, Deepanam,

Ruchyam, Vibhandham, anaha, Vistabda, Hruthshoola,

Gowrava, Shoola haram.

This is known in the markets as kala namak or black salt and is an artificial

product, prepared by mixing saindhava, haritaki, amalaki, and sarjakshara (sodium

carbonate), boiling these in water tilt evaporation is complete. Then the mess is

broken to pieces and sold.

SHUNTISynonyms : Viswabheshaja, Nagara, Ushna, Katubadra,

Sanskrit : Nagara

Telugu : Sunti

Hindi : Sonti

English : Dry Zinger

Latin Name : Zingiber officinale

Family : Zingiberaceae

Gana : Pippalyadi, Triptighna, Deepaniya, Vachadi,

Arshoghna, Sthanya Shodana, Trishna

Nigrahana, Sheeta prasamana,

Shodhaprashamana, Pachaneeya,

Haritakyadi varga

Rasa : Katu

Guna : Laghu, Snigdha

Veerya : Ushna

Vipaka : Madhura

Parts used : Rhizome

Karma : Kapha vata hara, Deepaniya, Ruchya, Hridya

Swarya, Vrishya.

Indications : Swasa, Kasa, Chardi, Shoda, Shoola, Agnimandya,

Vibanda, udara roga.

Chemical composition : Ginger contains volatile oil. Comphene,

Phellaudreve, Zingibarine, Cincol, borncol and

Ginger oil an purgent, an Alcoresin, Ginger,

Starch mucilage, potassium, oscolate, the

Essential oil and resin.

DADIMASynonyms Phalamla, Kucaphala, Sukavallabha, Kuttima,

Phalasadava, Raktabija, Karaka, Nila patra, Raktapuspa

Botanical name punica granatum

Family punicaceae

Telugu Danimma kaya

Hindi Anar

English pomegranti

Malayalam matalam

Tamil maduli

Ganas According Caraka – hridya, chardinigrahana

Susruta – Parusakadi

Vagbhata - Parusakadi

Types According to Kaiyadevara & Bhavamisra –

3 vareities of dadima

1. Svadvamla 2. madhura 3. amla

Rasa Kasaya. Madhura, amla

Guna Laghu, snigdha

Virya Ushna

Vipaka Madhura / Amla

Karma Tridoshahara, Hridya, Sukrala, Grahi,

Dosage Fruits juice 20-50ml. decoction 40-80ml. bark powder 3-

5g

Part used Fruit

Chemical compositon Fruit peels – Kannins, Punicatin. Seeds, Estrone, Danicic

Danicic acid

Stem – Malvidin, Pentosa, Ilucosides, Tannin

Ca, Mg, Na, Iron, Tamram V B1 B2.

PIPPALI

ynonyms: Kana, Krsna, Kola, Capala, Triksna Tandula,

Magadhi, Vaidehi, Usana, Soundi.

Botanial name: Piper longum linn

Family: Piperaceae

Hindi Pipal ,

English Long pepper

Telugu Pippallu

Tamil Tippili

Bengali Pipul

Malayam Tippali

Ganas: According to Susrutha Pippalyadi, Urdhvabhagahara,

Triyushana (Trikatu) Amalakayadi, Sirovirecana.

According to Vagbhata Pippalyadi ( A.S)

Past Used : Fruit, Root

Rasa Katu,

Guna Laghu, Snigdha Tiskhana

Virya Ushna,

Vipaka Madhura

Karma: Vata Slesmahara, Dipana, Vrusya, Rasayana.

Indications: Udara, pliharoga, jwara, kustham prameha, Gulma,Arsas, sula, amavata.

Major Chemical : Essential oil, Mono and Sesquiterperes,

Caryophyllore piperine, piplartine, piperlogumine,

piperlonguminine, pipernaline, pipelanguminine,

Pipernonaline, piperundecalidine, pipercide, secamin,

b- situsteror, four aristolactams (cepharanone B,

aristolactum (u).

PIPPALI MULA

Synonyms Kana, Krisna, Kola, Capala, Tiksnatandula, Magadhi, Vaidehi,

Sauna, Soundi

Botanical name Piper longumFamily Piperaceae

Telugu Pippallu

Hindi Pippala

English Long piper

Tamil TippiliGanas According to Kasahara, Hikkanigrahana, Seroverechana,

Vamana, Triptigna, Deepaniya, Shoola prasamana

According to susrutha – pippalyadigana

According to vagbhata – pippalyadi

Types According to susrutha & vagbhata havedefined 2 varietes pippali, Gajapippali

According to Rajanighantu – provides 4 varieties of

pippali 1. pippali 2. gaja pippali 3. simhapippale

4. Vanapippale

Gunas Text Rasa Guna Veerya VipakaCharaka Katu ushna

Bhava Katu snigdha Anushna Madhura

prakasa laghu

Dhanvantari Katu snigdha ushna Madhura

Nighantu laghuKaiyyadeva Katu snigdha Anushna Madhura

Nighantu laghu

Karma Udara, pliharoga, jwara, kusta, prameha, Gulma, Arsas,

Sula, amavata

Dosage: Powder ½ -1 gramsPart used: Fruit, root

Chemical compositon Essential oil, and sesquiterphon, caryophyllene (mainly),

piperine, piplartine piper longumine, sesamin, B-site sterol, Resin, Olatile oil.

DHANYAKA

Synonyms Kustumburo, Chatra, Vittunnaka, Dhanyaka

Botanical name Corundum satirum

Family Umbellifere

Hindi Dhaniya

Telugu Dhaniyalu

English – Coriander seeds

Ganas According to Caraka – Trsnaprasamana, Sulaprasanama

According to Susrutha – Guduchyadi

According to Vaghata - Guduchyadi

Rasa Kasaya, tikta,

Guna Laghu, snigdha

Veerya Ushna

Vipaka Madhura

Karma Tridosha hara, Deepana, Paachana, Grahi

Indications Jwara, Daha, Trusna, Chardi, Kasa, Swasa, … arsas

Dosage Fruit powdar 3-6 gms, cold infusion 20-30ml

Part used Fruit, whole plant

Chemical compositon Coriandrinol (glucoside) carotene cugenol, bergapten.

TEJO PATRA

Synonyms Tumburu, tejasvini, tejovati, vanaja, sourabha

Botanical name Zanthozylum ilatum

Family Rutaceae

Hindi Tejabala

English Toothache tree

Bengali Nepali dhana

Ganas According to Caraka Sirovircchana, katu skandha

Rasa Katu

Guna Laghu, ruksa

Virya Usna

Vipaka Katu

Karma Kapha – Vata hara, Kanthya, Dipana, Pacana

Indications Hrdroga, Mukha roga, Dantaroga, Kantha roga, Hikka,

Agnimandya, Arsas, Svasa kasa, Amavata, Apatantraka,

Udara

Chemical compositon Bark – herberine, xanthoplanine

Fruit – arginine, histidine, thujene

Root - spilanthol

TALISA PARTRI

Synonyms: Dhatripatra, patradhya, sukodara

Botanical name abes webbiana

Family pinaceae

Telugu & Tamil Talisapatri

Hindi & Bengali Tallispatra

English Indian silver

Ganas: According to susruta -sirovirecana

Types : According to Yadaviji trikamjit quoted 3 varieties

(1) T. baccata (2) A. webbiana (3) R. lepidotum

Rasa Tikta, madura

Guna Laghu, tiksna

Veerya Usna

Vipaka Katu

Karma: Kapha, Vatahara, Hridya, Dipana

Indications: Svasa, Kasa, Mukharoga, Ksaya, Chardi, Aruchi,

Agnimandya, Gulma, Raktapitta, Hikka

Chemical compositon: Abesin, n-triacontanol, B.Sitosterd, betuloside,

Riboflavonoid, betuloside

NAGAKESARA

Synonyms: Ahipuspa, loha. Kanakahva, kancanahvaya, kinijilkam,

kesaram, campeyam, natam, nagam, naga kinjilkam.

Nagapuspam, naga renuka, pinjaram, phani pannagam,

rukmam, suvarnam hemapushpam.

Botanical name Mescea ferrea

Family Guttiferae

Telugu Naga kesaralu

Hindi Iron wood of assam

English Naghas

Kannada Kanchana

Ganas: Susruta – Eladi, vacadi, anjanadi, priyangvadi ganas

A.S.S. – Eladi, vacadi, anjanadi, priyanvadi

A. Hrdaya – Eladi, vacadi, Anjanadi, priyanvadi ganas

Dhanvantaric nighantu – satapuspadi varga

Shodhala – satapuspadi varga

Kaiyadeva nighantu – osadhi varga

Types: 1. Mesua ferrea 2. ochro carpus longitolas

Rasa Kasaya, tikta

Guna Ruksha, Tikta, laghu

Virya usna/anusna

Vipaka katu

Karma: Kapha pittahara,. Pramathi, Grahi, Pachana, Visahara,

sothahara, kandughna, kusthaghna

Indications: Raktarsas, Raktatisara, Raktapradara, Kusta, Visarpa,

Jvara, Chardi, Vasti vikara, Vata rakta, Sopha, Vataroga,

Siro roga, Trsna, Visa roga, Kandu

Dosage: Powder of stamens 1-3g orally

Part used: Stamens

Chemical compositon Squalene, cycloartenol, campesterol, stigmasterol,

And bitosterol

MAREECHA

Synonyms : Mareecha, ushana, Vellaja, Krishna, Dharmapattana

Sanskrit : Mareecham

Telugu : Miriyalu

Hindi : Kalimirch, mirch

English : Black peper

Latin Name : Piper nigrum

Family : Piperaceae

Gana : Deepaniya, Shoola prasamana, Krimighna (Charaka);

Pippalyadi, Tryushana (Susrutha)

Rasa : Katu

Guna : Laghu, Teekshna, Guru (Ardra)

Veerya : Ushna

Vipaka : Katu Madhura (Ardra)

Parts used : Fruit

Karma : Kaphavatahara, Deepana, Avishya

Indications : Aruchi, Kasa, Peenasa, vishamajwara, Atopam.

It is also useful in coagulative disorders. It has

Bacteriostatic and fungistatic properties.

Chemical composition : Moisture 10.6, Protein 4.8, Fat 2.7,

Carbohydrates –13.7, Fibre 6.4, Mineral matter 1.8,

Calcium – 210, Phosphorous 17, Iron 2.4,

Thiamine 0.05, Riboflavin 0.04,

Nicotinic acid 0.2, Ascorbic acid 1 mg and

Vit. A. 1800 Im. And oxalic acid etc.

SWETA JIRAKA

Synonyms Ajaji, kana, jarana, dirgha jiraka

Botanical name cuminum cyminum

Family umbelliferae

Telugu JilakarraHindi Safed jeera

English Cuminum seeds

Marathi Jircin

Kannada Jirige

Ganas: Caraka – SulaprasamanaSusruta – pippalyadi

Vagbhata - pippalyadi

Types: According to Su. Su. 46 – Jiraka dvaya

In Dhanvantari nighantu – 4 vareities

1. Jiraka (Ajaji)2. Sukla jiraka (suklajaji)

3. Krishna jiraka (krsnajaji)

4. Vanya jirah (Bhhatphali)

According to shodala– 3 varieties (1) Upakunchika

(2) Sukla (3) KrishnaRasa Katu

Guna Laghu, ruksa

Veerya Usna

Vipaka Katu

Karma: Kapha – Vata hara, Dipana – Pachana, Grahi, Visya,Atisara, Gulma, Visa roga, Netra roga.

Indications: Krimi, Jirna Jvara, Adhmana, Kustha, Grahani, Atisara,

Gulma, Visa roga, Netra roga

Dosage: Fruit powder 3-6g

Part used: FruitsChemical compositon: cuminin, isoimperatorin, cuminaldehyde,

P-cymene, diacyl glycerol, imperatorin) paspharus,

calcium, iron. Vit A.C. etc. …

KRISHNA JIRAKA

Synonyms: Udgarasodhana, sugandha

Botanical name Carum carvi

Family Umbelliferae

Telugu Nallajilakarra

Hindi Syahajira

English Black caraway

Types Certain nighantu works described sexvareiteis

1. Sveta 2. Pita 3. Krsna 4. Suksma

5. Sthula 6. Vanyajeerakas

Rasa Katu

Guna Ruksa

Veerya Usna

Vipaka Katu

Indications Jvara, Chardi, Atisara, Gulma, Adhmana, Ajeerna

Dose Fruit powder 1-3 grms

Part used Fruit

Chemical compositon Essential oil, tricylo glycerols sterols, petroselinic acid,

essential oil – carone

CHOTI ELASynonyms Korangi, Dravidi,Tuttha, Triputa, Trtisthula

Ela – Bhadra Ela

Botanical name Electtaria cardamomum

Family Scitaminae

Telugu Chinna elakules

Hindi Chotiilaychi

English Lesser cardamom

Tamil Yelakka

Kannada Elakki

Ganas Caraka – Svasahara, Angamarda prasamana, Katuka

Skandha, Sirovirecana.

Types: All the texts have mentioned 2 variation of Ela

Sukshma Ela (E. cardamomam)

Brhat Ela (A. subulatum)

Rasa Katu, Madhura

Guna Laghu, ruksa

Veerya Sita

Vipaka Katu

Karma Kapha – vatahara, hrdya, sukra nasaka, deepana,

pachana

Indications Hridroga, svasa, kasa, mutrakricchra, chardi, sirahsula,

Arsas.

Dosa Powder 0.5-1 g

Part used Seeds

Chemical compositon Camphor citral, terpeneols, cymene, heptane sitosterol

TWAK

Botanical Name Cinnamomum Zeylanica Blume

Family Lauraceae

Hindi Dalchini

English Cinnamon

Telugu Lavanga patta

Tamil Ilayangam

Bengali Daruchini

Gujarati Taja

Synonyms: Utkata, tanutvak, darusita, varanga, svadvi, tvak,

Patta, bhrngam, kavaca, sakala, saihala , latapatra,

ramapriya

Ganas According to Susruta-eladi

According to Vagbhata Eladi, trijataka

Rasa Katu,

Tikta Madhura,

Guna Laghu, Ruksha, Tiksna,

Veerya Ushna

Vipaka Katu

Karma Vata pittahara, Sukrala, Balya, Vatarsas, Grahi

Indications Kandu, Amajirna, Aruchi, Krimi, Hridroga

Part Used Stem bark, oil

ANUPANA - TAKRASynonmys : Takra, Chachika, Dandahata, Gloha Gorasa,

Drava, Amla, Kekara, Madhita, Malima, Bhagna,

Sandhika, Gorasaja, Kalasheya, Vilodita, Arista,

Udasvitm Pramadhita, Ambare, Ghula, Kevala.

Telugu : Majjiga, Challa

Hindi : Chancha, Matta

English : Butter milk

Rasa : Madhura, Amla, Kashaya

Guna : Laghu, Rooksha, Grahi, Vikasi, Sara

Veerya : Ushna

Vipaka : Madhura

Karma : On dhoshas: Tridoshaharam

Indications : Agnimandyam, Pandu, Chardi, Grahani, Arshas,

Udara, Atisara, Aruchi, Krimi etc.

Description : It is not a ready made, but it is of from milk

through some of procedures.

Regarding its preparation, there are variations Samhita to samhita, on the basis

of preparation of Takra it is of 4 types (Dhanvantari-Nighantu and Susrutha) and 5

types (Bhava Prakasha). This Takra is one of the type among these.

Details: According to Bhava Prakasha

1. Gholam - By churning curd without water

2. Madhitam - By squimming the curd; excluding the outer layer and water.

3. Takram- Which is out of churned the curd by adding 1/4 part of water to it.

4. Udwasit - Which was by churned the curd which is long with half of the

water mixed.

5. Chachika - By squimming the curd with large quantity of water.

Where as Susrutha explained 4 types of Takra, but gave the description of the

Takra preparation, as it can be prepared by squimming the curd by adding Half

quantity of water to it.

"Seethakale agnimandye cha tada vatamayeshu cha

aruchow srothasam rodhe takram syadamruthopamam

....Tattu hanti pandu medo grahanyarso mutra graha bhagandaran"

"Na takra sevi vyadata kada china takra dagdhah prabhavanti rogah

yada suranam amrutam sukhaya tatha naranam bhuvi takramahu"

(Bhava prakasha)

According the modern system, there is slight difference between milk and butter milk.

Milk and butter milk same lactic Acid, whereas butter milk will not contain fat and

contains proteins as like as milk, because this is free from butter. Butter milk contains

lacto bacilie ie., useful bacteria, which helps in the modification of milk to curd. There

is change in the action also; milk can act as mild laxative, butter milk acts in reverse

way, which is helpful for diarrhiea, as we are saying in the society.

MODE OF PREPARATIONThe preparation of Bhaskara Lavana Churna was prepared as follows according

to Baisadya Ratnavali- Agnimandhya chikitsa Chapter.

Name of the drug Quantity

Samudra Lavanam 374 gms

Dadima Beeja 187 gms

Sauvarcha lavana 234 gms

Choti Pippali 94 gms

Pippali mula 94 gms

Dhanyaka 94 gms

Kalajeera 94 gms

Saindhava lavanam 94 gms

Bida lavanam 94 gms

Tejo patra 94 gms

Talisa patra 94 gms

Naga kesara 94 gms

Amla Vetasa 94 gms

Kali mareecha 47 gms

Swetha jeera 47 gms

Sunti 47 gms

Twak 24 gms

Choti Ela 24 gms

The above mentioned ingredients were collected in pure form the market. At

first, the all drugs were individually powdered finally and then mixed together in the

quantities mentioned above. The powder was weighed and several packets were

made each containing 2 gms of the drug. These were distributed to the patients.

Dose : 2 gms thrice a day

Time : Morning, Afternoon and evening after

principle meal

Anupana : Takra

Duration of treatment : 45 days

Indications: Pandu, Pleehavyadhi, Krimi, Ajeernya, Aruchi, Arshas, Shoda,

Amadosa, Gulma, Udara, Udararoga, Kshaya, Grahani, Kusta, Malabanda,

Hritishoola, Asmari, Sarkara.

By virtue of its propperties, the compound drug works in gastrointestinal, and

nutritional deficiency anemias.

MATERIALS AND METHODS

The materials required a clinical study on the effect of "Bhaskara lavana

Choorna" in the management of Pandu roga are

1. Patients

2. Parameters

3. Drug

1. Patients:

Selection of patients: Totally, 30 patients suffering from pandu are selected

randomly from the out-patient Department of Post graduate unit, Kayachikitsa

Department of Dr. B.R.K.R. Government Ayurvedic Hospital, Erragadda,

Hyderabad.

30 patients were examined thorougly according to the Lakshanas, Dasha vidha &

Ashta sthana pareekshas, and laboratory investigations. Those patients, who have been

elicited about rogi and roga pareeksha are noted in the proforma of special case sheet

of pandu roga, which is enclosed.

Inclusion criteria:

1. Pandutwa

2. Swetha nakhata

3. Agni mandhya

4. Aruchi

5. Kapha praseekam

6. Anga mardha

7. Brama

8. Jwara

9. Pindiko dwesta

10. Tandra

11. Alasya

12. Gowravam

13. Akshi koota sodha

14. Krimi kosta

15. Daha

16. Prabha heena

17. Swayathu

18. Palpitation

Exclusion of criteria:

1. Pateints suffers with cardiac diseases

2. Patients who are below 6 grams of haemoglobin

3. Hemorrhagic disorders Eg: Hemorroids

2. Parameters: The parameters that are used in assessing the results can be divided

into two categories.

a. Subjective parameters

b. Objective parameters

a. Subjective parameters:

The following have been taken as subjective parameters.

i. Relief of clinical signs and symptoms

ii. Appearance of Rakta saara lakshanas

b. Objective Parameters:

The following have been taken as objective parameters.

i. Hemoglobin Percentage

ii. Red blood cells count

3. DRUG REGIME: The drug Bhaskara lavana choornum a compound Ayurvedic

preparations, mentioned in Baisajya Ratnavali is selected to evaluat for anti

anemic activity.

THE METHODOLOGY:

a) The aim of the study:

Normalized the levels of Hb% in the Anemia.

b) Type of trial - open trial:

c) Mode of administration - oral

d) Method of administration:

Bhaskara lavana choornum started immediately after the

diagnosis of anaemia is confirmed

e) Dose of the drug

Bhaskara lavana choornum 6gms thrice a day. It is given in

three doses of 6 gms of the each principal meal.

f) Period of drug:

The progress of the patients is observed and recorded after every 21 and 45

days. This procedure is followed for duration 45 days. After the completion

of the duration, the results are assessed based on the observations.

g) Anupana - Takram:

The drug is given continuously for 45 days without any interuption and

Pathya, Apathyas are advised.

ASSESSMENT OF RESULTS:

After completion of the treatment the results are assessed in terms of Pravara,

Madhyama and Avara. The criteria adopted for the gradation of Lakshanas is shown

by the sign '+', and absence of Lakshanas is shown by the sign '-' .

The criteria adopted for this is given below:

1. PRAVARA: The result is concluded as Pravara when,

i. All the signs and symptoms present before starting the treatment are

relieved upto to 75% with no side effects

ii. Increase in Hemoglobin levels in between 12-15 grams.

iii. Increase in RBC count is between 4.5 and 6 million cells/cumm.

2. MADHYAMA: The result is concluded as Madhyama when,

i. The signs and symtpoms present before starting treatment are relieved

upto 50%.

ii. Increase in Hemoglobin levels is between 10-12 grams

iii. Increase in RBC count is between 3.5-4.5 million cells/ comm.

3. AVARA: The result is concluded as Avara when

i. The signs and symptoms relieved upto 25%.

ii. Increase in Hemoglobin levels is less than 10 grams

iii. RBCs count is less than 3.5 million cells/cumm.

Finally, all the information regarding the patients is noted down in various tables and

bars. These are presented in diagrams, so that records could be prepared properly. The

tables showing information regarding sex incidnece, mentioned in the chapter of

observation and results.

OBSERVATIONS

Thirty patients of Pandu attending the Postgraduate Kayachikitsa, department of

Government Ayurvedic Hospital, Erragadda, Hyderabad are randomly selected for

this clinical study.

The patients are classified into various groups according to the 1. Age, 2.sex, 3.

Diet, 4. Economical status, 5. Signs and Symptoms, 6.Occupation, 7. Ahara and 8.

Prakriti.

The Signs and Symptoms, Hemoglobin Percentage and Red blood count before the

treatment are recorded. The condition of the patients is reviewed after every 15 and 45

days of treatment. It is continued up to a duration of 45 days and the observations

were recorded.

Table 1: According to Sex:

Sl.no. Sex No. of cases Percentage

1 Male 4 13.33

2 Female 25 83.33

3 Children 1 3.33

Out of thirty cases 25 cases were females, 4 cases were male and 1 male

children were seen.

No. of Patients

Male

Female

Children

3.3%

83.33%

13.33%

Table 2. According to Age:

S.No. Age group No. of male No. of female Total Percentagein year patients patients

1 0-10 1 0 1 3.33

2 11-20 0 3 3 10

3 21-30 1 9 10 33.33

4 31-40 3 9 12 40

5 41-50 0 4 4 13.33

30 patients were classified according to the ages as shown in table 2.Maximum cases

was seen in 31-40 year age group.

Table: 3 According to Diet:

S.No. Diet No. of male No. of female Total Percentagepatients patients

1 Vegetarian 2 11 13 63.33

2 Mixed 3 14 17 36.66

In the present study the vegetarians are 63.33%, ( 13 out of 30) and mixed diet were seen 36.66% (17 out of 30).

Table 4: According to Economical status:

0

1

2

3

4

5

6

7

8

9

0-10 11-20 21-30 31-40 41-50

M ale

F em ale

Age in Years

0

2

4

6

8

10

12

14

V egetarian M ix ed

M ale

Fem ale

Type of diet

Table 4: Accoridng to Economical Status :S.No. Economical No. of male No. of female Total Percentage

patients patients

1 Poor 4 15 19 63.3

2 Middle 1 8 9 30

3 Rich 0 2 2 6.66

The patients were observed as per socio-economical status based on their

monthly income. Out of 30 cases 19 casses were poor, 9 cases were middle classes, 2

cases were seen rich.

Table 5: According to Occupation:

S.No. Occupation No. of male No. of female Total Percentagepatients patients

1 Labour 3 15 18 60

2 Student 1 6 7 23.33

3 Sedentary 1 4 5 16.33

Out of 30 cases, 18 casses were labour, 7 cases were Student and 5 sedentary

cases were seen.

Table 6: According to Prakriti:S.No. Prikriti No. of male No. of female Total Percentage

patients patients

1 Vata 2 6 8 26.66

2 Pitta 1 5 6 20

3 Kapha 2 14 16 53.33

In the present study 16 casses were Kapha predominent prakriti, 6 casses were

Pitta predominent prakriti and 8 cases were seen Vata predominent prakriti.

Table 7: Symptoms present Before and After the treatment:

S.No. Symptoms BT After treatment Percentage

1 Pandutwam 30 28 93.33

2 Sweta nakhata 30 25 83.33

3 Agni nasanam 30 30 100

4 Aruchi 24 21 87.5

5 Angamardha 24 18 75

6 Kapha praseka 24 20 83.33

7 Brama 10 5 50

8 Jwara 15 13 86.66

9 Pindiko dweshta 20 14 77.77

10 Tandra 20 16 80

11 Alasya 20 16 80

12 Gowravam 25 22 88

13 Akshikoota sodha 4 2 50

14 Krimi kosta 4 2 50

15 Daha 13 10 33.33

16 Prabha heena 20 14 70

17 Swayathu 5 3 60

18 Palpitation 20 13 68.42

In the present study symtpoms and signs seen before and after the treatment

MASTER CHART, SHOWING DATA IN RELATION TO PANDUROGA

After treatment Before treatmentS.No

Name Age Sex

RegNo.

Diet Econo-micalStatus

Occupation

Prakrati 0 days 21 days 45 days Result

Hb RBC Hb RBC Hb RBC1 Rajyalaksh

mi30 F 11185 Mixed Middle Sedentar

yPitta pre. 7.0 3.2 8.2 3.8 9.4 3.2 Avara

2 Vijayalakshmi

35 F 11117 Vegetarian

Poor Student Vata pre. 6.3 2.8 7.8 3.1 8.8 3.1 Avara

3 VijayaMarry

40 F 21492 Mixed Poor Student Kaphapre.

10.5 3.4 12.1 3.1 13.1 5.1 Pravara

4. Madhavi 25 F 11186 Mixed Middle Labour Kapha pre. 8.0 4.2 9.2 4.4 11.8 3.8 Madhyama

5. Mahaboobvali

40 M 14667 Mixed Poor Labour Kapha pre. 11.5 3.2 12.3 4.9 13.2 4.8 Pravara

6 Eswaramma

40 F 19184 Vegetarian

Poor Labour Kapha pre. 10.2 3.1 11.6 3.3 13.3 3.5 Pravara

7 Ramadevi 34 F 21497 Mixed Poor Labour Kapha pre. 9.0 4.2 9.4 4.4 11.6 4.5 Madhyama

8 Rajamma 45 F 21496 Mixed Rich Student Pitta pre. 10.0 3.8 8.6 3.9 9.8 3.9 Avara9 Jayasree 31 F 13120 Vegetaria

nPoor Sedentar

yKapha pre. 9.8 3.4 10.9 4.3 13.1 4.5 Pravara

10 Asiyabegum

27 F 5553 Mixed Middle Labour Vata pre. 8.0 2.9 8.8 3.6 9.8 3.8 Avara

11 Lakshmi 45 F 11582 Vegetarian

Poor Labour Kapha pre. 10.0 4.1 9.8 4.7 11.8 4.3 Madhyama

12 Tulasi 45 F 11118 Mixed Poor Labour Vata pre. 10.2 3.8 12.2 3.3 13.0 4.6 Pravara13 Sabeyabe

gum17 F 11135 Vegetaria

nMiddle Labour Kapha pre. 10.0 3.2 11.6 3.2 13.2 3.5 Pravara

14 Sudershan 6 M 11272 Vegetarian

Poor Sedentary

Vata pre. 7.0 3.2 9.2 4.3 10.0 3.5 Avara

15 Sarada 24 F 14287 Vegetarian

Poor Sedentary

Kapha pre. 8.5 3.8 9.4 3.9 10.8 3.8 Madhyama

16 Kirankumar

22 M 8505 Mixed Middle Student Pitta pre. 10.5 3.4 12.6 4.6 14.0 5.1 Pravara

17 Sunitha 23 F 8936 Vegetarian

Poor Student Kapha pre. 10.5 3.4 11.6 3.1 12.8 4.8 Pravara

18 Sailakshmi 24 F 8507 Mixed Poor Student Vata pre. 10.5 3.8 11.4 4.3 12.9 5.2 Pravara19 Seetamma 40 F 11116 Mixed Middle Labour Pitta pre. 9.8 3.6 9.2 3.8 12.0 3.7 Madhya

ma20 Faridabeg

um42 F 17771 Vegetaria

nPoor Labour Pitta pre. 11.0 3.2 12.8 3.6 13.1 4.8 Pravara

21 Reshma 20 F 19862 Mixed Rich Labour Kapha pre. 9.8 2.7 10.2 3.5 13.8 3.5 Pravara22 Kalpana 20 F 7716 Vegetaria

nPoor Sedentar

yVata pre. 10.5 3.3 10.9 3.7 13.6 4.8 Pravara

23 Madhuri 26 F 18873 Mixed Poor Labour Kapha pre. 9.5 3.2 10.6 4.0 12.9 4.6 Pravara24 Lingaiah 32 M 21722 Vegetaria

nPoor Labour Vata pre. 9.5 3.9 11.8 3.1 12.9 4.5 Madhya

ma25 Anitha 30 F 22646 Vegetaria

nMiddle Labour Vata pre. 11.0 3.8 12.8 3.3 12.9 3.5 Pravara

26 Ananta 34 F 21316 Mixed Middle Labour Kapha pre. 10.5 3.5 11.4 3.1 13.0 4.8 Pravara27 Taribai 35 F 11114 Mixed Poor Labour Pitta pre. 7.0 2.7 10.8 4.6 13.1 4.8 Pravara28 Amribai 30 F 11115 Mixed Middle Student Kapha pre. 7.3 3.8 11.2 3.8 13.2 5.0 Pravara29 Lakshmi 32 F 11583 Vegetaria

nPoor Labour Kapha pre. 8.2 3.1 10.3 4.0 12.9 4.8 Pravara

30 Yallamaiah

40 M 24705 Vegetarian

Poor Labour Kapha pre. 10.1 3.9 11.4 3.6 11.8 4.2 Madhyama

Final Result: After the completion of 45 days of treatmentPravara 60% (16 Female and 2 Male) Madhyama 23.66% (5 Female and 2 Males), Avara

16.66% (4 Female, 1 Male)

Table 8: Haemoglobin levels before treatment

Hb levelsin grams

3.1-4 4.1-5 5.1-6 6.1-7 7.1-8 8.1-9 9.1-10 10.1-11 11.1-12 12.1-13

Males 0 0 0 1 0 0 1 2 1 0Females 0 0 0 2 5 2 8 8 0 0Total 0 0 0 3 5 2 9 10 1 0Percentage 0 0 0 10 16.7 6.6 30 33.2 3.33 0

In the present study the haemoglobin levels ranged from 6 to11.5 gms/dlbefore the treatment.

Table 9 : Heamoglobin levels after 21days oftreatment

Hb levelsin grams

6.1-7 7.1-8 8.1-9 9.1-10 10.1-11 11.1-12 12.1-13 13.1-14

Males 0 0 0 1 0 2 2 0Females 0 1 3 5 6 5 5 0Total 0 3 3 6 6 7 7 0Percentage 0 3.3 10 20 20 23.33 23.33 0

Hb levels showed gradually increased with in 21days from the starting day of treatment.

1

2

0

5

0

2

1

8

2

8

1

00

1

2

3

4

5

6

7

8

Males

Females

0

1

0

3

1

5

0

6

2

5

2

5

0

1

2

3

4

5

6

Males

Females

6.1-7 7.1-8 8.1-9 9.1-10 10.1-11 11.1-12 Hb levels (gms)

Table 10 : Heamoglobin levels after 45 days of treatment.

Hb levelsin grams

8.1-9 9.1-10 10.1-11 11.1-12 12.1-13 13.1-14 14.1-15

Males 0 1 0 1 1 2 0Females 1 3 1 4 8 8 0Total 1 4 1 5 9 10 0Percentage 3.33 13.3 3.33 16.66 30.0 33.2 0

Hb levels achieved to maximum levels with in 45 days of treatment.

Table 11: RBC levels before treatment.

RBC levels inmill/cumm

1.6-2.0 2.1-2.5 2.6-3.0 3.1-3.5 3.6-4.0 4.1-4.5 4.5-5.0 5.1-5.5

Male 0 0 0 3 2 0 0 0Female 0 0 4 11 7 3 0 0Total 0 0 4 14 9 3 0 0Percentage 0 0 13.3 46.66 30 10.0 0 0The RBC levels before the study of treatment ranged from 2.7 to 4.2 million/cumm.

7.1-8 8.1-9 9.1-10 10.1-11 11.1-12 12.1-13 Hb levels (gms)109

0

1 1

3

0

1 1

4

1

8

2

8

0

1

2

3

4

5

6

7

8

Males

Females

0

43

11

2

7

0

3

0 00

2

4

6

8

10

12

Male

Female

8.1-9 9.1-10 10.1-11 11.1-12 12.1-13 13.1-14 Hb levels (gms)

2.6-3.0 3.1-3.5 3.6-4.0 4.1-4.5 4.6-5.0RBC levels (millions/cumm)

110

Table 12: RBC levels after 21 days of treatment:RBC levels 3.1-3.5 3.6-4.0 4.1-4.5 4.5-5.0 5.1-5.5 5.6-6.0in mill/cumm

Male 1 1 1 2 0 0

Female 9 10 4 2 0 0

Total 10 11 5 4 0 0

Percentage 33.2 36.7 16.66 13.3 0 0The RBC levels showed gradually increase with in 21 days from the starting day oftreatment.

Table 13: RBC levels after 45 days of treatment:RBC levels 3.1-3.5 3.6-4.0 4.1-4.5 4.5-5.0 5.1-5.5 5.6-6.0in mill/cumm

Male 0 0 2 3 1 0

Female 6 5 3 9 1 0

Total 6 5 5 12 2 0

Percentage 19.98 16.66 16.66 40 66 0RBC levels showed best results after 45 days from starting day of treatment.

0

1

2

3

4

5

6

7

8

9

1 0

3 . 1 - 3 . 5 3 . 6 - 4 . 0 4 . 1 - 4 . 5 4 . 5 - 5 . 0 5 . 1 - 5 . 5

M a l e

F e m a l e

0

1

2

3

4

5

6

7

8

9

3 . 1 - 3 . 5 3 . 6 - 4 . 0 4 . 1 - 4 . 5 4 . 5 - 5 . 0 5 . 1 - 5 . 5

M a l e

F e m a l e

RBC levels (millions/cumm)

RESULTSThe results of the treatment of assessed periodically after 21 and 45 days till the

completion of the duration i.e.45days. the results are tabulated according to the signs

and symptoms, Hemoglobin percentage, RBC levels, percentage of result etc.

The results are assessed and graded as Pravara, Madhyama and Avara according tothe parameters mentioned in materials and methods.

Table No.1: Responsed based on Sex

S.no Sex Pravara Madhyana Avarage1 Male 2 2 02 Female 16 5 43 Children 0 0 1

The present study comprises 13.33% of adult males (4out of 30), 83.33% of

adult females (25 out of 30) and 3.33% (1out of 30) of male children. Out of these

6.7% (2out of 5) among males, 60% (16 out of 25) adult females got best result.

RBC levels (millions/cumm)

Table No.2: Responce based on Age.s.no. Age

(years)Pravara

Male FemaleMadhyama

Male FemaleAvara

Male Female1 0-10 0 0 0 0 1 02 11-20 0 3 0 0 0 03 21-30 1 5 0 2 0 24 31-40 1 6 1 2 0 15 41-50 0 2 1 1 0 1

The present study comprises of different age groups. The youngestbeing 6 years and the oldest has 45 years. Out of these, 31-40 years age got best result,followed by 0-10, 11-20,21-30,31-40 and 41-50 age groups, 2 out 5 adults Male patientsachieved best results followed by 2 madyama and one avara patients. 16 out of 25 adultsfemales got best results, followed by 5 madhyama and 4 avara patients.

2

16

0

2

5

0 0

4

1

0

2

4

6

8

10

12

14

16

MaleFemaleChildren

Pravara Madhyama Avara

112

RESPONSE BASED ON SEX

0 0

1

3

00

6

2 2

7

3

1

2 2

1

0

1

2

3

4

5

6

7

Pravara

Madhyama

Avara

0-10 11-20 21-30 31-40 41-50 RESPONSE BASED ON AGE

Table.3: Response based on Diet.s.no Type

DietPravara

Male FemaleMadhyama

Male FemaleAvara

Male Female1 Vegitarion 0 7 2 1 1 12 mixed 2 11 0 3 0 2

In the present study vegetarians are 40% (12out of 30) and mixed diet are 60%(18out of 30). Out of these 43.3% (13 out of 30) mixed diet got better results than that ofvegetarians 23.3% (7out of 30).

Table No.4: Response based on Economic status

Economic Pravara Madhyama Avara TotalStatus Male Female Male Female Male Female

Poor 1 2 3 10 0 3 15

Middle 1 5 0 3 0 0 9

Rich 0 2 0 0 0 0 2In the present study, the incidence of poor is more than that of middle class and rich

6.66% (2 out of 30) among rich, 60% (9 out of 30) among middle class, and 63.33 (15out of 30) among poor.

Table No. 5: Response based on symptoms/signs

S.No. Symptoms/Signs No.of Improved Partially Notcases improved respond

1 Pandutwam 30 25 4 1

2 Swethanakhata 30 20 5 5

3 Agnimandhya 30 25 5 0

4 Aruchi 23 18 3 3

5 Kaphapraseekam 23 16 2 6

6 Angamardha 23 18 2 3

7

13

3 32 2

0

2

4

6

8

10

12

14

Vegitarion

Mixed

Pravara Madhyama Avara

113RESPONSE BASED ON DIET

7 Brama 10 4 1 5

8 Jwara 15 10 3 2

9 Pindikodwesta 18 12 2 2

10 Tandra 20 14 2 4

11 Alasya 20 15 1 2

12 Gowravam 25 20 2 3

13 Akshikoota sodha 4 6 2 2

14 Krimikosta 4 0 2 2

15 Daha 30 15 10 5

16 Prabhaheena 20 10 4 6

17 Swayatha 5 3 1 1

18 Palpitaion 19 11 2 5

In the present study, pandutwa is an important symptoms that got considerabale

improvement. 25 out of 30 pateints showed best results with complete relief, 4 with

partial improvement and 1 case showed little response towards treatment. Other

important symptoms such as agnimandhya, aruchi, Gowravam, and kaphapraseekam

also showed greater response to the treatment. The list of sign and symptoms before

the treatment and after the treatment is tabulated above.

Table No.6: Hemoglobin levels before treatment

Hb levels Males Females Total Percentage %

Pravara 0 0 0 0

Madhyama 4 9 13 43.33

Avara 1 16 17 56.66

In the present study, the hemoglobin levels ranged from 6 to 11.5 grams/dl

before the treatment. Patients with very poor hemoglobin levels are 56.66% and

patients with average anemia are 43.33%.

0

2

4

6

8

10

12

14

16

P rava ra M adhy am a A vara

M ale

F em a le

Table. 7: Hemoglobin levels after 21 days treatment

Hb levels Males Females Total Percentage

Pravara 2 4 6 20

Madhyama 2 12 14 46.7

Avara 1 9 10 33.3

Hemoglobin levels showed gradually increase with in 21 days from the starting

day of treatment. The poor haemoglobin patients before the treatment decreased from

56.66% to 33.3%.

Table.8: Hemoglobin levels after 45 days of treatment.

Hb levels ingms

Males Females Total Percentage%

Pravara 2 16 18 60.00Madhyama 2 5 7 23.33Avara 1 4 5 16.66

Hemoglobin levels achived to maximum levels with in 45 days of treatment.60% of the

patents (18 out of 30) turned non-anemic, where as 23.33% of the patients (7 out of 30) got

moderate results, and 16.66% of the patients. (5 out of 30) did not respond much to the

treatment.

10

12

14

16

Table No.9: RBC levels before treatment

RBC levels Males Females Total Percentage

Pravara 0 0 0 0

Madhyama 2 11 13 43.33

Avara 3 14 17 56.66

The R.B.C. levels before the starting of treatment ranged from 2.7 to 4.2 mill/cumm.

The Avara group of patients are 56.66% (17 out of 30) and moderate group are

43.33% (13 out of 30).

Pravara Madhyama Avara

0

2

4

6

8

1 0

1 2

1 4

P ra va ra M a d h y a m a A va ra

M a le

F e m a le

Table 10: RBC levels after 21 days of treatment

RBC levels Males Females Total Percentage

Pravara2 2 2 4 13.33

Madhyama 2 15 17 56.66

Avara 1 8 9 30

The R.B.C. levels showed gradually increase with in 21 days from the starging day of

treatment. The Avara group of patients before the treatment decreased from 56.66% to

13.3%.

TABLE NO: 11

RBC levels after 45 days of treatment

RBC levels Males Females Total Percentage

Pravara 3 11 14 46.7

Madhyama 2 9 11 36.6

Avara 0 5 5 16.66

RBC levels showed best results after 45 days from the starting day of treatment. The

Avara group of patients with very low RBC levels before the treatment decreased

from 30% to 16.66%, Madhyama group of patients decreased to 56.66% to 36.6% and

Pravara group of patients increased to 13.33% to 46.7% with the increase in RBC

levels.

10

12

Table No. 13: Final Result After Completion of Result

Results Males Females Total Percentage

Pravana 2 16 18 60.03%

Madhyama 2 5 7 23.33%

Avara 1 4 5 16.66%

After 45 days of treatment, there is significant decrease in the clinical symptoms,

increase in the hemoglobin and RBC levels, decreased in E.S.R. levels and patients

felt comfortable.

4

6

8

10

12

14

16

Male

Female

Responced based on After Completion of Treatment

6.6%

16.6%

Table Showing statistical parameters of Hb% and RBC

S.No. Parameters Mean SD SE t P

1 Hb% 2.6 0.8 0.14 1.8 <0.1

2 RBC 0.9 0.6 0.11 1.3 <0.1

After doing paired 't' test the vaoues obtained are mean for Hb% is 2.6, SD is

0.8, SE is 0.14%, 't' is 1.8 and 'p' is <0/1.

After doing paired 't' test the values obtained are mean for RBC is 29.6, SD is

0.6, SE is 0.11, 't' is 1.3 and 'p' is <0.1.

Male

Pravara

MadhyamaAvara

Female

Pravara

Madhyama

Avara

3.3%

6.6%

6.6%

13.3%

16.6%

53.33%

DISCUSSION

Pandu roga is one of the most common disease described in Ayurveda. The

detailed description about it in all aspect is available in most of the Ayurvedic

classics. It is a highly prevalent disease. Ayurveda offers a number of effective

formulations in the management of pandu roga. The compound drug "Bhaskara lavana

churna" with takra has been selected for the clinical trial to prove its efficacy in

raktalpatha conditions.

Pandu roga being a common ailment in developing countries specially in India,

the prevalence is seen in both sexes and age groups. The females and childrens are

more prone disorder. So the present clinic trial is conducted to find out an effective

treatment for anaemia.

The etiological factors of pandu roga found in Ayurveda can be studied under 4

groups Ahara, Vihara, Manasika, and nidanurthakara Rogas, due to the excessive

intake and practice of above factors.

The disease pandu is manifested due to the predominance of pitta in the

pathogenisis of the disease, though vatadi tridoshas are vitiated in the samprapti. The

consumed food, which has the proparties of kshara, amla, lavana, ati ushna etc, acts as

predisposing and precipitating factors responsible for manifestation of the disease.

These factors cause prakopa of pitta gunas i.e. Sneha, teekshna, ushna, laghu, visra,

sara and drava. The increased dravaguna affects Agni and reduces its teekshnata.

This mandagni cannot digest the food that is consumed. Thus the agnimandhya forms

and which is followed by inadiquate rasadhatu formation, leeds to raktalpatha i.e.

pandu roga.

Pandu roga lakshanas mentioned in Ayurveda are dhatu shaitilyam, raktaalpatha,

etc. Which are the cardinal symptoms of Anaemia. The reduced

hemoglobin and packed cell volume conditions in anaemia of modern science

are comparable with raktalpata condition of pandu roga.

The compound drug i.e. "Bhaskara lavana choornam has been selected. for this

study as it is non contraversial, non-toxic, easily available and economical.

The ingredients present in this preparation; Dadima, pippali, pippali mula,

Dhanyaka, Teja patra, Naga kesara, Amla vetasa, Krishna jeeraka and Swetha Jeera,

Sunti, Twak, Sukshma ela, Samudralavanam, Sauvarchan lavana, Saindhava lavana,

Bida lavanam have properties of Rasayana, Deepana, Pachana, Hridya, Balya,

Tridosha shamaka, Ruchyam, Sodhaharam, Tridosha shamaka. These properties are

considered for their effective management of Pandu roga.

The Dadima, pippali, pappli mula, Dhanyaka, jeeraka, Tejo pathra and Twak

contains the property of krimigna. So are responsible for the elimination of worm

infestation, which is the one of the cause of the pandu roga.

The Balya property of swethajeeraka assists in alleviating the dhatukshya and

ojokshaya, present in Pandu Roga.

The statement "Samanyam Ekatwa karam" mentioned in ayurvedic classics is

justified by asrik prasadana propperty of Dadima, Shunti, Jeeraka in pandu roga.

Takram, which is used as anupana in the clinical trial, is Tridoshashamaka and

agnideepana. It can also prevent dhamani pratichaya because it is srotho sodhaka as

well as vatahara drarvya.

The gradual increase in the Hb levels is observed with in the first weak of

treatment and it reaches the maximum levels in 45 days of duration. This may increase

in Hemoglobin levels is attributed to increased production of intrinsic factors by

Bhaskara lavana churnam. The increased production of intrinsic factor also

contributes to the increased up take of lohamsa in ahara and oushadha. Improvement

in the abhyavaharana as well as and jarana shakti are also observed immediately

with in the first weak of treatment, because this preparation contains Maricha,

Shunti, Jeeraka, Amlavetasa, Nagakesara Twak, Ela and Pippali which has agni

deepana and pachana proparties.

In two pateints, purgation is noticed on the first two days of tretment. This was

thought as adverse effect noticed during the study. It got relieved after adjustment of

the dose in those pateints.

The pale discoloration of the skin, conjuctive, and nail is converted to normalcy,

with gradual increase in Hemoglobin and R.B.C. levels. This was completely

achieved by the end of the treatment.

The increased production of intrinsic factors also contributes to the increased

uptake of lohasma in ahara and oushadha. This is due to direct action of Dadima,

Shunti, Jeeraka on Amasaya, Yakrit and Ranjakapitta.

Significant decrease in E.S.R. levels is noticed in the study. This is due to anti

inflamatery, antiseptic and anodyne properties of Bhaskaralavan churnam.

Thus the reduced rakta in the body is agian replanished by the treatment with

Bhaskara lavana churnam .

The conditions of the patients before and after treatment are assessed based on

the parameters (both subjective and objective). The patients are followed up for 45

days and progress is noted as per systematically prepared special case sheet of pandu.

The results are assessed as Pravara, Avara and and madhyama based on clinical

picture and laboratory investigation.

The prevelence of pandu roga according to present study found more in females

83.33%, (25 out of 30). Than the males 16.66% .

Among these cases (7 out of 25) females were suffering with Desfunctional

uterine bleeding. It leads to Anemia. After the treatment 3 cases had moderate

relief and other 4 cases were mild relief. 1 out of 30 case was seen in pregnacy.

After the treatment she had moderate relief.

In 1 out of 30 cases one male Patient under went truma by bike accident recently.

After the treatment the patient got moderate relief.

In 1 out of 30 cases, the male child have PICA. It was improved after 45 days of

treatment.

56.66% Non-vegetarians got better results than that of vegetarians according to

diet.

Out of 30 cases 31-40 years of group got best results followed by 21-30 11-20,

age 41-50, 0-1 year age groups.

The incidence of poor is more than that of middle class and rich, because

malnutritional diet, irregular food habits. In these leads to anaemia. After the

treatment 63.3% (15 out of 30) among poor, showed better result according to socio-

economical status.

Pandutwa is an important symptom has shown considerable improvement, 70%

patients showed better results with complete regular.

Other important symptoms agnimandya, Swethanakhta; Aruchi, Gowravam,

Kapha prasekam showed greatly responce to the treatment due to action of drugs

Pippali, Mareecha, Shunti, Amlavetasa, Jeeraka, Tejoptra and Talisa patra of

Bhaskaralavana churna having Deepana, Pacchana and Rasayana properties.

Raktalpatha may have also responsed to the treatment due to Dadima. Jeeraka,

and Shunti which contains Iron.

The pathogenesis, Sareera, Drug aspect, Observations and results are discussed

elaborately under respective heading. The results are analysed statistically and

conclusions are drawn.

CONCLUSIONThe conclusions drawn from the present study are listed here under:

1. The patients of poor economical status are more prone than the middle class

and the rich.

2. The patients consuming katu and Amla rasapradhana aharas are more prone

to the disease than those who consume madhura rasa ahara.

3. In pandu roga, vitation of pitta is vriddi, but not ksheena.

4. Females are more prone to this disease than males.

5. Pregnant women are commonly afflicted with the disease.

6. The people residing in urban areas are more prone to the disease than those

residing in suburban and rural areas.

7. People with Arshas, Asrigdara and malaria are more prone to the disease.

8. The drug Bhaskara lavana churna is effective in Pandu, when the vitiated

doshas are mainly vata & Kapha.

9. The age group of 21.30 are more prone to the disease. Followed by 31-40

and 11-20. Reproductive age group in India is between 21 and 30 years in

general. This may be the reason for occurance of the disease. It is also seen

that the age group of 11-20 is also prone to the disease because of their

growing period and less intake of nutritious food is the real cause for

occurance of the disease.

10. The drug Bhaskara lavana choornam is effective in pandu, when the vitiated

doshas are mainly vata and kapha.

11. The drug can be administered with takra in pitta prakriti patients.

12. The symptoms like Dourbalyata, Aruchi, Kasa, Swasa, Shotha, Mandagni,

Ajeerna, Asya vairasyam are relieved with the drug effectively.

13. Hemoglobin and RBC levels gradually increased with oral intake of 2 grms

thrice a day of Bhaskara lavana churna with in a span of 45 days.

14. ESR levels decreased, Hb & RBC levels increased to normal range in

majority of the patients by the end of the treatment, thus proving the

efficiency of the drug.

15. It is necessary to adjust the dosage of the drug and duration of treatment

according to symptoms and signs, prakriti and koshta of the patients.

16. In a patient with history of krimi roga, oral Administration of Bhaskara

Lavanam along made him pass ascaris through faeces. This is a signifcant

finding which also indicated that Bhaskara lavana choornam could be

administered in krimi roga.17. Finally, it can be safety concluded that Bhaskara lavana churna is an effective

and cheap remedy for the most common aliment Pandu. It shoudl be usedroutienly in the management of pandu especially on mass level as it worksout to be economical.

SUMMARY1. INTRODUCTION: The disease is most common in Indian population and in

the both the sexes, especially in pregnant women. It can be compared to the state

of decreased hemoglobin and RBC levels i.e., Anemia of modern system of

medicine. The drug Bhaskara Lavana Choorna is administered to 30 patients,

attended to Out Patient Department of P.G. unit of Kayachikitsa department and

"The clinical Study on the Effect of Bhaskar Lavana Choorna on Panduroga." is

carried out.

2. HISTORICAL ASPECT: The description of the disease is being carried out

since ages. Harima, Halima and Vilohita are the terms used as synonyms for

Purana and Mahabharata. Charaka, Susruta, Vagbhata, Laghutrayee and

subsequent authors of Sangraha Granthas described the disease and chikitsa in

detail. On the other hand, Anemia is derived from Greek words 'an' and 'emia.' It

was previously termed as 'demarbo verginia' by Johnanna Lange in 1554.

3. SHAREERA (Kriya and Rachana): The main doshas involved in the

pathogenesis are Pachaka Pitta, Ranjaka Pitta, Vyana vata, Bhrajaka pitta, and

Kledaka Kapha. The dhatus involved in the pathogenesis are Rasa, Rakta,

Mamsa, Sarakta Medas and Ojus. The organs involved are Yakrit, Pleeha,

Hridaya and Amashaya. Decreased levels of Hemoglobin and RBC is noticed in

Anemia and is related to blood, its contents, Hemopoiesis, and its physiology.

4. THE DISEASE: The disease is classified as Vataja, Pittaja, Kaphaja,

Sannipataja and Mritbhakshana Janya Pandu Roga. Anemias are classified

according to pathology as Microcytic, Macrocytic or Normocytic anemias.

5. NIDANA: The factors that vitiate pitta such as usna, teekshana, amla, lavana,

katu aharas are the causative factors for Pandu Roga. The etiological factors of

anemia are Hemorrhagic, Dyshemopoietic, Hemolytic and Aplastic anemia.

6. POORVA ROOPA: Twak Sphotana, Shteevana, Gatra Saada, Koota Shodha,

Avipaka, Hridaya spandana, Swedabhava, Shrama, Anga Saada, Alpagni and

Shareera Krishatwa are the poorva roopas of Pandu Roga.

7. ROOPA: Alpa Rakta, Dhatu Shaithila, Kopana, Alpa Vak, Hata Anala, Shrama,

Bhrama are some of the important roopas of pandu roga. Rasa vaha Sroto dusti

Lakshanas are also seen in pandu roga. Pallor of cheeks, nails and mucous

membrane, fatigue and lassitude are some of the important clinical features of

Anemia.

8. SAMPRATI: Vitiated Pitta vitiates rasa Dhatu and causes the disease. The

vitiated also pitta affects the rakta dhatu causing Alpa rakta and leads to the

disease. The consumption of Mrit is also the causative factors for Pandu.

9. UPADRAVAS AND ARISHTA LAKSHANAS: Aruchi, Pipasa, Chardi,

Jwara, Shodha are important Upadravas. Shopha, swasa, Trishna etc., are the

Arishta Lakshanas.

10. SADHYASADHYATA: Pandu roga becomes asadhaya when it reaches chronic

state and occurance of Upadravas & Arishta Lakshanas is seen.

11. chikitsa krama: Chikitsa Krama of pandu roga includes the following steps.

1. Nidana Parivarjana

2. Snehana Chikitsa

3. Shodhana Chikitsa: Vamana and Virechana

4. Samana Chikitsa: Herbal, Mineral and Compound preparation

Anupanas like Takra, Madhu, Ksheera and Ghrita etc., are used for

the many preparations.

12. PATHYA APATHYA: Those ahara, aushadha, viharas, which are suitable and

not suitable to the patient and the disease as well are Pathyas and Apathyas

respectively.

13. DRUG ASPECT: The drug Bhaskara Choornam is selected for clinical study

keeping in view the disease, patients, safety, chikitsa sutra and the availability of

the drug.

14. MATERIALS AND METHODS: Patients, parameters, and drugs are the

materials required - parametery include subjective symptoms and objective

signs. The dose of drug 6 gms t.i.d. along with takra after principal meal. The

duration of treatment is 45 days.

15. OBSERVATIONS: The conditions of the patient before the treatment and along

with the course of the treatment for every 21 days is observed and recorded for

period of 45 days in total.

16. RESULTS: The results of the treatment are drawn based on the observations

made. The results are assessed as Pravara, Madhayama, and Avara, as per the

clinical symptoms and laboratory results.

17. DISCUSSION AND CONCLUSION: Pathogenesis, Shareera, Drug aspect,

Observations and Results are discussed elaborately in various angles and

conclusions are drawn based on the same.

DR. B.R.K.R. GOVERNMENT AYRUVEDIC COLLEGE/HOSPITALERRAGADDA, HYDERABAD – 500038

DEPARTMENT OF KAYA CHIKITSA – P.G. UNITSPECIAL CASE SHEETON PANDU ROGA

Name of the Patient: Regd No:Age: Sex: Married/Unmarried: Occupation:Social /Financial status:

Address:

ROGA PAREEKSHA

1. CHIEF COMPLAINTS WITH DURATION:

2. ASSOCIATED SYMTOMS:

3. HISTORY OF PRESENT COMPLAINT:

4. HISTORY OF PREVIOUS ILLNESS: Vishama Jwara / Asrigdara / Arshas/Atisara/ Arbuda/ Krimi/ Allopathic drugs/ Shastra Karma

5. FAMILY HISTORY: Suffers of Pandu – Mother/Father/ Grand parents/Others

6. PERSONAL HISTORY:a) Diet: Shakahara / mamshahara:

b) Habits: Madyapana/Dhoomapana/ Tea/ Tobacco:

c) Appetite: d) Sleep: e) Urine:

f) Bowels: g) Menstruval history:

II. PHYSICAL EXAMINATIONa) Height: b) Weight:c) Build: d) Tongue:e) Nails: f) Skin:g) Palms of hands: h) Conjunctive:i) Mucous membrane: j) Oedema:j)

III. CLINICAL EXAMINATION:

a) BP: b) PR:

c) Respiratory rate: d) Heart:

e) Lungs: f) Liver

g) Spleen: h) Temperature

ROGI PAREEKSHA:1. SHADVIDHA PAREEKSHA

1) Prakriti: Vata/Pitta/kapha2) Vikriti: Dosha – vata / pitta / kapha

Dooshya – Rasa / Rakta / mamsa / medo/Asthi/majja/sukra3) Sara: Pravara / Madhyama / Avara4) Satwa: Pravara / Madhyama / Avara5) Samhanana: Susamhana / Madhyama / Asamhana6) Pramana: Pravara / Madhayama / Avara7) Satmya: Pravara / Madhyama / Avara8) Aharashakti: Abhyavaharana shakti – Pravara / Madhyama / Avara

Jarana – Pravara / Madhyama / AvaraJatharagni – Pravara / Madhyama / Avara

9) Vayah: Bala/ Yavana / Sampoornatha / Parihari / Vriddha.10) Vyoyama shakti: Pravara / Madhyama / Avara

Desha – Jangala / Anupa / SadharanaKala – Seetha / Ushna/ Varsha

2. ASHTASTHANA PAREEKSHA:1. Nadi: Vata/ Pitta/ Kapha/ Dwandaja / Sannipataja. Sankhya - /min.

Gati – kshipra / manda

2. Mala: Varna – Peelha / swetha / Prakrita

Sama / Nirama / Vibandha.

Pravritti: Adika / Prakrita/ Alpa

3. Mootra: Varna – Peeta / Swetha / Prakrita

Pravritti – Adhika / Prakriti / Alpa

Pramana – Adhika / Prakrita / Alpa

4. Jihwa: Amayukta/ Niramayukta

5. Twak: Varnam – Pandu / Peeta / Rakta / Ruksha / Snigda

6. Shabda: Karnaksweda / Shabda asahana / Prakrita

7. Drik: Harswa drishti / Deerga drishti

Netravarnam – Swetha / Peeta / Atipeeta / Ruksha / Snigda

8. Akriti: Ksheena / Sthoola / Madhyama

Sodha – Mukha / Hasta / Pada

SROTHAS INVOLVEDPrana/ Anna/ Udaka/ Rasa/ Rakta/ Mamsa/ Medas/ Asthi/ Majja/ Sukra/ Mootra/ Purisha/Sweda/ Cheshta/ Samgna/ Manovaha/ Arthavavaha

LAKSHNAS OF PANDU ROGAVataja pandu Pittaja Pandu Kaphaja panud Mridbhakshana

panduLakshnas B A Lakshanas B A Lakshanas B A Lakshnas B Aa)Rukshatwa(paleness &Dryness)Twak MutraNetra NakhaJihwa

b) Toda(PrikingSenstion)

a) Peethatwam(yellowishness)MalaMutraNakhaJihwaTwak

d) Daha(burningsensation)

a) Suklatwam(Whiteness)TwakMutraJihwaNakhaNetra

b) Swayathu(Swelling)

a) Sotha(Swelling)AkshikutaBruMedraGudaYoni

b) Rakta,Kaphamisrita,

c)Kampa(Tremours)

d) Anaha(Distension)

e) Branma(giddiness)

f) Swasa(Shortnessof breath)

g) Dourbalya(debility)

c) trishna(Thirsty)

d) Jwara(Fever)

e) Bhinnavit/Atisara

c) Tandra(Drousiness)

d) Alasya(Slugishness)

e) Atigourava(Heavyness)

f) Aruchi(Dysphasia)

Vamana(Diarrhoea)

Nutritional Infection Endocrine Drugs

Worm infestion Bleeding disorders Genetic disorders

S.No. Ist day 21st day 45th day

1 CBP: Hb%

RBC

2 ESR

3 Stool examination

4 Urinary analysis

5 Ultra sound abdomen

6 Chest X-ray

7 Others

VYADHI VINISCHAYA:

TREATMENT UNDERTAKEN

a) Drug prescribedb) Dosage schedulec) Duration of treatment given

FINAL CONCLUSION

a) Cure in percentageb) Response to treatmentc) Special not if any

RESULT

a) Pravarab) Madhyamac) Avara

Sign. Of the Co-guide Sign. Of the Guide Sign. Of the PG.Scholar

INFORMED CONSENT

I, ................................... Son/ daughter / wife of ................................. am

exercising my free will to participate in above study as a subject. I have been informed

to my satisfaction by the attending physician the purpose of clinical evaluatin and the

nature of the drug-treatment. I am also aware of my right to opt out of the treatment

schedule at any time during the course of the treatment.

Schedule initiation Patient Signature

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Kalpadruvam Dev Bahadur Culcutta, 1808

44. Shabda ratnavali - -

45. Shabdasthoma Sri taranath Veedanyantra PRess,

Mahanidhi Takravachaspathi Calcutta, 1976

46. Sarangadhara Sarangadhara V. Ramaswami Sastrulu

Samhita Mishra & Sons, Vavilla Press,

Madras, 1952.

47. Susruta Samhita V. Ramaswami Vavilla press, Madras

Shastrulu 1954

48 Susruta Samhita Ambikadatta Choukambha Samsthan,

Sastry Varanasi, 4th Edition 1979

49 The Indian Materia Dr. K.M. Nadkarni Popular Book Depot,

Medica Bombay.

50 The Iron Deficiency Gibbson 1963

& Pernicious Anaemia

51. The Wealth of CSIR, New Delhi, 1969

India, Vol, III, VIII & IX

52. Vaidhya Chintamani Indrakanti Venkateshwara Book

Vallabhacharyulu Depot. Sec'bad. 1955

53. Vangasena Hearaja Sri Sri Venkateshwara

Krishnadasa Mudranalaya, Bombay

Shreshti 1876.

54. Yoga Ratnakara-I Yeturu Nellore, 1939.

Srinivasacharyulu

Formation and destruction of red blood cells,And the recycling of hemoglobin components.

INGREDIENTS OF BASKARA LAVANA CHURNAM

SOWVARCHA LAVANAM SAMUDRA LAVANAM

SAINDHAVA LAVANAM

BIDA LAVANAM

BHASKARA LAVANA CHURNAM

TAKRAM

RED BLOOD CELL