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A clinical study on the effect of Bhaskara lavana choornum in pandu Roga, K. SUNEETHA, Department of Kayachikitsa, PG unit Dr.BRKR Govt. Ayurvedic College, HYDERABAD

A clinical study on the effect of Bhaskara lavana choornum in pandu Roga, K. SUNEETHA, Department of Kayachikitsa, PG unit Dr.BRKR Govt. Ayurvedic College, HYDERABAD

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    Pandu kc016 hyd Pandu kc016 hyd Document Transcript

    • 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 guideDr.V.VIJAYA BABU M.D. (Ayu.), Professor, P.G. Unit of Kaya Chikitsa., For hisexcellent 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 timelysuggestions, thought provoding leads ideas and support in Completing this thesiswork. I am very thankful to my co-guide Dr. RAMALINGESWARA RAO garu,Technical Assistant and Lecturer for their precious suggestions and help through outthe 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 RetiredProfessor, Dr. M.L. NAIDU garu for their valuable suggestions and encouragement. I am also thankful to teaching staff, Post graduate department of Kaya Chikitsaespecially Dr. VIJAYA LAKSHMI garu, Dr. NAGESWARA BABU garu, for theirprecious 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, whichdirected 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.GuruMurthy, Mr. Prabhakar, Mr. Sambasivam, Prasanth, Chinnamma, BhagyaLakshmi, Suneela, Sujatha, Seshanka, Surya Teja, AND Ganesh for the valuabesupport 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 especiallyDr. 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 methroughout this thesis work directly and indirectly. I special thanks to Dr. Yashoda MD (Ayu.) lecturer, in B.R.K.R. AyurvedicCollege for her valuable suggestions and encouragment. I sincerely thankful to Smt. Mamatha & Mr. Chakravarthy, VS GRAPHICShelps me in the computerized of the thesis. Hyderabad February 2008 (Dr. K. SUNEETHA )
    • CONTENTSPART – I PRELIMINARY PART 1. Intorcution 1 2. Historical Review of the diseasePART - 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 69PART - III CHIKITSA 1. Chikitsa krama 71 2. Pathyas and Apathyas 78PART-IV DRUG REVIEW 1. Criteria for selection of Drug 80 2. Description of individual drugs 82 3. Mode of preparation 99PART V CLINICAL STUDY 1. Materials and Methods 101 2. Observations 105 3. Results 112PART - VI 1. Discussion 121 2. Conclusion 125 3. Summary 127PART - VIISpecial case sheet for Pandu Roga130 2. Bibliography 134
    • INTRODUCTION Ayurveda is origin from vedas, mainly from Adharavana veda. According toAyurveda, definition of health includes both physical and mental well being andtreatment was mentioned for both Swastha in order to preserve health and Atura inorder to treat the disease. Chaaya and prabha are associated with skin and are based on the condition ofBhrajaka pitta. The discoloration like the colour of ketaki dooli, swetha, peeta, haritaetc., are the manifestations of pathological process caused not only by the etiologicalfactors 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 Indiabut also world wide. The panduroga is included under the heading of"Varnopalakshita Roga" ie., Varna pradhanya disease. It is known since ancienttimes. The disease is referred as Vilohita, Harima, and Halima in vedas and susruthanamed it as Panaki, Laghavaka and Kumbhahwa. William D.Whitney an eminent authority of vedic literature compared vilomawith anaemia. It is the commonest disease irrespective of age, sex and religion. It isprevalent in women, pregnant in specific. As the prevalance of the disease is morecomparatively research studies are needed to evalutate proper eradication procedure,with the help of the system of medicine which has been existing since many centuriesi.e. Ayurveda. The iron deficiency is the commonest nutritional dificiency world overand 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 ofmedicine, in which the haemoglobin concentration falls bellow the accepted normalrange due to the failure of haemoglobin synthesis and other conditions mentioned innidana and sareera. In particular where unhygienic, low socioeconomic and faultyfood 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 rightfrom ages. The Ayurvedic classics have mentioned a number of effective formulations fortreatment of pandu roga keeping in view of the above factors, the present studyentitled as "A clinical study on the effect of Bhaskara lavana choornum in panduroga" is carried out. The efficasy of this formulation in pandu roga can be justified by its indicationin Alpa rakta condition explained in the pages that follow. The preparation BhaskaraLavana churna is taken from Agnimanandya chikitsa Adhyaya of BhaishadjyaRatnavali. 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 patientdepartment of post graduate unit of kayachikitsa, Dr. B.R.K.R. Govt. Ayurvediccollege / Hospital, Erragadda, Hyderabad. The drug Bhaskara lavana churna is triedon 30 patients and results are assessed periodically. The results are encouraging, which are discussed in length, in the chapter ofresults seperately, the entire work is devided into VII parts, covering all the aspects ofthe disease. Pandu roga and Drug Bhaskara Lavana Churnam.Part I consists of introduction and historic review of the disease. Part II consists ofvarious aspects of the disease such as definitions, synonyms, classification, sareeraRachana, Sareera kriya, Nidana, Samprapti and other aspects. Part III consists ofchikitsa krama of pandu roga in general. Part IV consists of various aspects of drugs indetail. Part V consists of clinical study, under which, materials and methods,observation and results are included. Part VI consists of discussion, conclusion andsummary. Part VII consists of special case sheets and Bibliography.
    • HISTORICAL REVIEW Ayuevedia is the most ancient system of medicine among the different systemsof medicine existing. Vedas are apourshayas. Vedas are the oldest knowledge books known to menaccording to Indian thought. So, it would be appreciable to explore the history rightfrom the period of Vedas to present period. On the scale of time, next to Veda arePuranas, Upanishads and Brahmanakas, Samhitas, Sangrahas, Nighantus andArvacheenakala Grandhas. Now, let us consider some of the points related toPanduroga mentioned in different texts/literature/knowledge available till date in astepwise manner under the following headings. 1. Veda Period 2. Purana Period 3. Samhita and Samgraha Period 4. Avracheena Period1. Vedic Period: In Vedas there are many references about the disease Pandu.Rigveda: Pandu roga has been mentioned under the name Harima. Suryanamaskarasand prescribed as its treatment in Rigveda.2. Yajurveda: In Yajurveda there is a reference about Pandu. A reference from thisveda quoted that there is some relation between yakrit, kloma and pitta in relation toPanduroga. Charaka and Susruta has elaborated this point in detail by stating that themoolasthana of raktavaha srotas lies with yakrit and pleeha and the predominant doshaassociated with Pandu is pitta.3. Atharvanaveda: This veda reiterated the same as above. There are references likeVilohita, Harima, Halima which can be taken as synonyms of Pandu. The significanceof sun rays is stressed in Atharvana veda for changing the colour in Pandu roga.Another reference from Atharvanaveda advocates godugdha as a remedy forPanduroga.
    • 4. Pouranika kala:Garuda Purana, valmiki Ramayana and Agni purana have alsomentioned about Pandu roga. In Garuda purana lohachoorna with takra anupaana isprescribed especially for Pandu patients, and Nidana, Lakshanas, Pathyaapathyavicharanas are also explained in detail. Mahabharata states that the Hastinapura king had suffered from Pandu rogawhose name itself is Pandu Raju. He acquired the disease as a curse from a saint. Thisexplains the karmasiddhanta of Panduroga. King Pandu acquired sterility due to PanduRoga as a complication and he even died of the disease.5. Samhita & Sangraha kala: This is the golden period of ayurveda, since most ofthe Ayurvedic Classics like Charakasamhita, Susruthasamhita, Bhelasamhita,Hareetasamhita, Kasyapasamhita took shape in this period. These samhitas are thebasis of Ayurveda that is being practiced throughout the world. Panduroga has beendescribed 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 4 th Even the works such as Chakradatta, vangasena, Yogaratnakara,Bhaishajyaratnavali, Basavarajeeyam, Madhavanidanam and Sarangadhara samhitaalso give a detailed description of Pandu roga.
    • We can find references of a number of medicinal plants that are proved to beuseful in Panduroga in Dhanvanthari, Kayyadeva and Astanga nighantus. The authorof Vidhyachintamani Srimad Indrakanta vallabha charyulu stated that Pandu is asenapathy (chief of army) for the disease Kshaya. With the advent of Rasakala, some mineral and metallic preparations replacedthe herbal drugs, after shodana and marana. Rasaratnasamucchaya, Rasapadhati andother literatures on Rasashastra have thousands of preparations which are prescribedfor 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 vilohitamentioned in Vedas to anaemia. Hippocrates, the father of modern medicine in 460BC, described anaemia likesymptoms such as pallor and weakness. he attributed these symptoms to the chagnesof blood. Anaemia, in those days, was found predominately in virgins and was hencecalled 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 pulsationof the temporal vessels and dysponea on climbing stairs or dancing. This illness waslater termed Chlorosis and clinical use of iron was first initiated in 17th century byThomas Sydenham. Dr. Grambiel andral succeeded in describing the changes of bloodmicorscopically in Anaemia during 1797-1876. Also the work of Thomas Addison, during the same period contributed to thediscovery of one of the type of anaemias - The Addisions Anemia. This is later ontermed as Perinicious Anemia, After the efforts of Dr. Wilks in 1855 and Dr.Biermers 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 consistingof liver and beef, which are rich in iron. this showed considerable improvement ofPerinicious Anemia. However, they could not provide enough explanation for thesame. 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 inPhysiology and Medicine for their work concerning the treatment of Anaemia withliver. In 460BC Hippocrates also explained the importance of consumption of liver incombating anaemia during pregnancy. The same was also recommended by Charakaand Susrutha in 500 B.C. Now-a-days, there are many clinical, pathological, and diagnostic technologiesavailable in regards to Anaemia. As per Modern system of medicine, anaemia is ofmany types. It is being treated on the whole by supplement of Iron and its source inthe form of daily nutrition or in medicines which would be seen in detail in the topicsthat follow, as and when in need. This disease is prevalent in most communities due tovarious causes and yet a lot has to be achieved. The above review clearly indicates that Pandu is blood related disease, itsrelation is to Raktavaha srotomoolas has long back been mentioned and Ayurvedicphysicians were aware of the disease and its management since vedic period. Thushistory of Pandu and its corelated disease. The Anaemia of Modern system ofmedicine 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, Samsthanaand 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 vijayarakshit 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 calledpandu roga “Pandu shabdena swetatwa mabhideeyate: (Dalhana on S.Su.33/23) Dalhana, the commentary on susrutha samhita, started that pandu means whitecolour. “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 anailment associated with colour of patient.
    • SYNONYMS OF PANDU ROGA The 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 vibhashyate lakshana 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 orless and “emia” which means blood condition. Pandu (Anaemia) is a condition ofreduction 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 calledpanduvarnam. Normal adult male – 16 gms/dl Normal adult female – 14 gms /dl Anaemia is also said to be present in adults if the "Hematocrit (packed RBC) isless than 41% in males and 37% in males. Anemia is also seen in patients in whom theRBC is less than the normal. Normal adult male RBC – 5,20,000/cumm. Normal adult female RBC – 4,700,000/cummReferences: 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 vedicliterature there is no evidence of any classification regarding pandu roga. Onlysynonyms such as Harima, Halima, Vilohita are found on the literature. The detail description of pandu roga and is classification starts from Ayurvedicsamhitas 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 theMridbhakshanaja pandu and he explained for this as Mridbhakshanaja pandu mayinclude in vatadi doshaja pandu’s according to the rasa pradhanata of mrit1. In Haritha samhita “Rukshana” pandu is appears of mridbhakshanaja pandu. Theterm Rukshana may be used, because mridhbhakshanaja pandu mainly cause theRukshanatwa of the body2. Astanga sangrahas and many other texts followed the same order while susruthamentioned 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 sannipatajaPandu 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 MritbhaskhanajanyaPandu 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 ASPECTClassification: 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 anaemiaIII. 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 etc 4. 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 nutritionalanaemia, megaloblastic anaemia of pregnancy, pernicious anaemia1. Normocytic anaemia: There is reduction in RBC with if all a slight increasingMCV, MCH remains normal throughout. Eg. Sudden loss of blood due to theantipartum, post partum haemorrhage2. Microcytic normocytic anaemia: There is reduction in red cell volume, Hbcontent with less MCH eg. Actute and chronic inflammatory disease3. Microcytic hypochromic anaemia: Reduction in RBC volume and Hb contentand 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 8 th 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 diseaseoccurs 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 kaphaII. The Dhatus are involved in Pandu Roga are: 1. Rasa 2. Rakta 3. Mamsa 4. Medas 5. Asthi 6. MajjaIII. 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 isimportant in the study of the pandu roga. Abrief description of the above factors isneeded.
    • 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 andtiryaggamana v. Jrimba pravartana vi. Anna aswadana vii. Sroto vishodhana viii. Dhatu tarpana b. Samanavata: The Vayu that gives strength to Pachaka pitta is called samanavayu. Location: It resides near pachaka pitta. It courses between Amashaya andPakwashaya. It is also been said that it also occurs in Sweda, Rakta, and Ambu vahasrothas. Gunas: In general, it possess all the gunas of vayu. Karma: The important function of Samana Vayu is to strengthen Jataragni. Thusit helps in the digestion of food. After digestion, it divides ahara into saara and Kittabhaga. According to Vagbhata, samana vata does ahara graham (accepts food) intokoshta, anna grahana, Saara-Kitta vibhajana and it pushes the Kitta into Pureesha vahasrothas.
    • 2. Pitta a. Pachaka Pitta: We know that the entire body depends on the food weconsume and the way it is absorbed and assimilated into the body tissues. The type ofpitta that does the above said functions is dependent on Pachaka pitta. This pitta alsoregulates digestive capacity, Dhatu parinama and provides nutrition for the body. Thisis called as Pachakagni, Koshatagni, Antaragni, Kayagni, Jataragni or Agni,depending upon the context. It has also been said that vitiation of pachaka pitta leadsto disease. Location: Pachaka pitta is located in between Amashaya and Pakwashaya. Theregion between amashaya and pakwashaya is termed as Grahani and it containsPittadhara 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, thedravatwa guna in pachaka pitta is less when compared to other pittas. Karma: It has wide range of fuctions. The important functions among them areas 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 orRanjakagni 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 circulatedthrough Yakrit and Pleeha and transforms it into Rakta Dhatu. This act is evencontrolled by Rakta Dhatwagni. c. Bharajaka Pitta: The temperature of the body as well as the colour of the skin are dependent onBhrajaka pitta. “Twakstham bhrajakam bhrajana twachaha” (A.H.S. 12-14) Location: Skin is the site of Bhrajaka pitta. Avabhasini, which is the first layerof 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 uponthe 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 theform 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 resultinto 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 thePathogenisis of Pandu roga samprapti. Pandu is included under rasa prodoshajadiseases. Location: Hridaya and Dasadhamanis. It circulates through out the body alongwith 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 subjectedto jatarapaka and Rasadhatwagnipaka. It stays in each dhatu for a period of 3015kalas. It circulates upwards like Agni, downwards like jala and transversely likeshabda. 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 therakta dhatu with the help of Ranjaka pitta. Therefore the Ranjakapitta plays anessential 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 etiologicalfactors. The characteristic features of Pandu quite opposite to the characters ofShuddharaktapurusha. 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. Itcirculates 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 ofpure blood. Pramanas: Eight Anjalis. Gunas: Anushna, Seetha, Snigdha, Guru, Visra and Asamhata and Gunas ofPanchamahabhutas. 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 andrakta Varna is regarded as Shudda Raktasaarapurusha.Ojus: The involvement of ojus is specifically mentioned in Charaka Chikitsa 16thChapter. As the formation of all Dhatus is impaired in the disease Pandu, theformation 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 substancesabsorbed from the gastrointestinal tract to the tissues, returns CO2 to the lungs andother products of metabolism to the kidneys, functions in the regulation of bodytemperature, and distributes hormones and other agents that regulate cell function. The circulatory (or) vascular system is divided for descriptive purpose into twomain parts 1. The Lymphatic system 2. The Blood circulatory system The Disease pandu roga is similar to the disease Anaemia of modernmedicine. Anaemia is concerned with lower haemoglobin levels in the blood. It is acondition 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 communicationbetween 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 proteinsclotting factors, inorganic salts, nutrient materials, hormones, enzymes, antibodies andgasses.
    • 2. Formed elements: Contains cell and cell fragments (45%) – Red blood cells orErythrocytes, white blood cells or leucocytes and platelets or thrombocytes presentless 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 majorFunction of RBC also known as erythrocytes is to transport haemoglobin, which inturn carries oxygen from lungs to tissues. Haemoglobin is present in RBC in humans. RBC have other functions besides transport of hemoglobin. They contain largequantities of carbonic anhydrase, which catalyses the reactions between water andCO2, increasing the rate of this reversible reaction to as much as several thousandtimes. This makes it possible for water in blood to react with huge CO2 and therebytransport it to lungs from tissues in the form of BiCarbonate Ion (HCO3).
    • The Haemoglobin in the cells is an excellent Acid – Base buffer and isresponsible for most of buffering power of whole blood. Size and shape of RBC: Normal RBCs are bioconcave discs having a meandiabmeter of about 7.8  and a thickness of about 2.5 mm at the periphery and 1mm mof less in the center. The shape of RBCs can change remarkably as the cells passthrough capillaries. Concentration of RBCs in the blood: The average volume of the red bloodcells 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 cellfluid, when the heamatocrit ( the percentage of blood that is in the cells- normally 40to 45%) and the quantity of haemoglobin in each respective cells are normal. Thewhole blood contains an average of Haemoglobin in Men – 14-16 gms/dl Women 12-15 gms/dl Infants – 14-20 gms/dlEach 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 are produced. l Liver spleen & Lymphnodes: During mid trimester of gestation – the liver is the main organ or production of RBC, although ressonable number of RBC are produced by spleen and lymph nodes. l Bone marrow: During the last months of gestation – RBC are produced exclusively 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 occupy most of the cavity. Beyond this age RBCs are produced by marrow of membraneous bones such as verterbrae, sternum, ribs and ilia. Origin and development of Red Blood Cells: The first cell that can beidentified as belonging to the red blood cells series is the proerythroblast. Once theproerythroblast has been formed, It divides several more times, eventually formingmany mature red blood cells. The first generation cells are called Basophilicerythroblasts, which then develops into a Proerythroblast (Normoblast) erythroblast,the first cells in the sequence that begins to synthesize hemoglobin. The polychromatophilic erythroblast next develops into an acidophilic erythroblast, in whichhemoglobin synthesis is at a maximum. In the next stage, the acidophilic erythroblastejects is nucleus and becomes a reticulocyte. The reticulocyte in turn becomes anerythrocyte (or) mature red blood cell. Once the erythrocyte is formed, it leaves themarrow and enters the blood stream.Formation and destruction of red blood cells and recycling of hemoglobincomponents. Red blood cells live only about 120 days because of the wear and tear inflictedon their plasma membranes as they squeez through blood circulation worn-out redblood cells are removed from circulation and destroyed by fixed phagocytic
    • macrophages in the spleen and liver. The globin and heme protions ofhemoglobin are split apart. Globin is brokendown into amino acids, which can bereused to synthesize other proteins. Iron removed from the heme portion. Associateswith a plasma protein called transferring, which transports iron in the blood stream. Inmuscle fibers, liver cells, and macrophages of the spleen and liver, iron detaches fromtransferring and attachs to iron storage proteins called ferritin and hemosiderin.Upon release from a storage site or absortion from the gastrointestinal tract, ironattaches to transferring. It is then transported to bone marrow, where RBC precursorstake it up through receptor – mediated endocytosis. For use in production of newhemoglobin molecules. Erythropoiesis in red bone marrow results in the production ofred 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 theblood and is transported to liver with in the liver, bilirubin is secreted by liver cellsinto bile, which passed into the small intestine. Again which passed into the largeintestine, in large intestine bacteria convert bilurubin into urobilinogen. Someurobilinogen 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 brownpigment called stercobilin, which gives feces their characteristic colour.Erythropoietin: The principal factors that the stimulates red blood cell production isa circulating hormone called erythropoietin. Tissues oxygenation is a basic regulator of RBCs production. Any condition thatcauses the quantity of oxygen transported to the tissues to decrease ordinarly increasethe rate of RBCs production.Other factors controlling erythropoises: The red cells are constantly beingdestroyed and regenerated. Certain factors are necessary for the formation of redblood cells. They are:1. Diet: Proteins are very valuable supply of essential amino acids for the synthesis ofhemoglobin.
    • 2. Metals: Iron, Copper, Cobalt, Calcium and Manganese. Iron is essential for theformation of hemoglobin. Copper, Cobalt, Calcium and Manganese are indirectlyhelpful in the formation of RBCs.3. Bile satls: Presence of bile salts in the intestine is essential for the proper absorptionof these metals.4. Endocrine glands: Certain glands such as thyroid and adrenal glands are havingunknown role in the metabolism of RBC.s5. Vitamins: Vitamin C, B complex, and Folic acid are helpful in the formation ofRBCs.Erythropoietin and its formation: Erythropoietin is a hormone found in circulatingblood. It is a glycoprotein with molecular weight of 34,000. In the absence oferythropoietin, hypoxia has little or no effect in stimulating RBCs production. On theother hand, when Erythropoietin system is functional, hypoxia causes marked increasein Erythropoietin production, and this in turn enhances RBCs production until hypoxiais relieved.Role of kidneys in the formation of erythropoietin: In normal person, about 90% ofall erythropoietin is formed in the kidneys. Mainly, the liver forms the remainder. Therenal tubular epithelial cells secrete the erythropoietin because anemic blood is unableto 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 theproduction of proerythroblasts from hemopoietic stem cells in the bone marrow. Oncethe proerythroblasts are formed, the erythropoietin causes these cells also to pass morerapidly through the different erythroblastic stages than normal, further speeding up theproduction of new cells. The rapid production of cells continues as long as the personremain in low oxygen state or unitl enough RBCs are producted to carry adequateamounts of oxygen to the tissues.Formation of RBCs – Requirement of Vitamin B12 and Folic Acid: For the finalmaturation 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 requiredfor the formation of Thymidine Triphosphate, an essential building block of DNA.Therefore, lack of either of these causes diminished DNA and consequently, failure ofnuclear formation and division. Therefore, it is said that Vit. B12 and folic aciddeficiency 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 isfound mainly in green vegetables, liver and whole grains. The reference nutrientintake is 50g/day. Following its uptake by the mucosal cells, folate undergoesreduction and methylation. Once, it arrives in the liver, the methyl derivative is takenup, undergoes demethylation and the tetrahydrofolate is converted into polyglutamylforms with 4,5 or 6 residues. The polyglutamyl forms contstitute a store of thevitamin. Prior to release from the store, and into the circulation, the compound isconverted to N-methyl-derivative, from which all but one of the glutamyl residues isremoved.Folate deficiency: The members of society most liable to folate deficicney arepregnant women and the elderly. It is now recognized as being good practice toadminister folate supplements as soon as pregnancy is confirmed and to continue untilterm. 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 Spinabifida and anencephaly is reduced by as much as two-thirds. Later in the pregnancythe supplementation is to prevent folate deficiency in the mother, which can easilyarise as foetal demands cause depletion of maternal foliate stores. Less commonly, folate defienciey may be seen in alcoholics, in those patientsbeing treated with anticonvulsants and in individuals with intestinal malabsorptionconditions.VITAMIN B12 : Normal daily requirement of Vitamin B12 is 1-2 g/day. It enters intofood 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. Insaliva 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 thestomach. In the more neutral surroundings of the duodenum the R-binders undergohydrolysis, thereby releasing their Vitamin B12 .Intrinsic factor: Maturation of the cell depends on a number of factors, especially thepresence of vitamin B12 and folic acid. These are present in sufficient quantity in anormal diet. Containing dairy products, meat and green vegetables. If the absorptionof vitamin B12 depends on a glycoprotein called intrinsic factor secreted by parietalcells in the gstric mucosa. Thus very little or none is absorbed in cases with perniciousanaemia and after gastrectomy as the intrinsic factor absent. In main it is produced bythe body of the stomach. It is glycoprotein.The essential property of the intrinsic factor is its ability to bind Vit B12 and to act asa carrier. The presence of hydrochloric acid probably facilities this binding in thestomach 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, becauseof both digestive enzyme action in the gut and failure of its absorption. The transportof Vitamin B12 in the plasma occurs in association with two major bindingproteins:Transcobalamin I and Transcobalamin II.
    • IRON METABOLISM: Metal ion used most frequently in association of proteins often include iron intheir 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 foralready association with, and dissociation from its binding sites on protein i.e., itskinetic liability. The complexes formed, however, are thermodynamically stable. Themajor 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 rangefrom 1.0 to 3.2 mg/day, and this must derive from, dietary srouces/Although iron iswidely distributed in foodstuffs, only a proportion, which may be 10% or less, isabsorbed from the diet. For this reason, the minimal amount needed to be ingesteddaily 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 smallintestine particularly the duodenum. Dietary iron is absorbed through the mucosalcells as Ferrous (Fe++) form. Iron in diet is mostly present as a ferric (Fe +++) statewhich is reduced to ferrous form during absorption. Vitamin C, glutathione and aminoacid – SH groups help in reduction of ferric to ferrous form. After entering themucosal cell as Ferrous form, the iron molecules are rapidly reconverted into ferricstate. A ferric iron as ferric – hyroxy phosphates combines with a protein, apoferritinwith a protein apoferritin of. The mucosal cells with the formation of iron-phosphorusprotein 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 juicehelps absorption. The gastric HCL helps reduction from ferric form to ferrous. Partialgastrectomy often leads to iron deficiency anaemia. Calcium small amount decreasesthe formation of insoluble iron phosphates and thus helps absorption but large amountof Ca. inhibits iron assimilation. Vitamin – C increases the absorption of iron fromfoods, possibly reducing the ferric iron into the ferrous state.5. Time taken for absorption: The rate of absorption is determined by the ironrequiremen for Hb synthesis. In anaemic cases, after a single dose of iron, a rise ofserum iron takes place in 30 minutes, reaching its maximum in 3-5 hours and returnsto normal in about 12 hours. Maximum absorption is completed in 18 hours.6. Iron storage: iron is incorporated into the iron-storage protein Ferritin, inenterocytes, but the main stores of iron in the mammalian body are in the liver andspleen. In addition to storage as Ferritin, iron can also be found in a form calledHaemosiderin inside the liver.7. Iron balances: For an adult to stay healthy, the amount of iron lost each day muchbe replaced by an equivalent intake. Young rapidly growing children, on the otherhand, 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 mostlyconsidered.8. Iron excretion: Iron is unique among the trace elements in that there is noexcretory system for eliminating the metal from the body. This is generally lostthrough erythrocytes in bleeding. The routes for loss of iron may be classified aseither physiological or pathological.9. Physiological Iron Losses: The adult male and the non-menstruating female loseabout 1 mg iron per day. Of this total, 50-60% is accounted for by loss from thegastrointestinal tract, due either to biliary excretion or to the shedding of mucosalcells. The remainder is lost with hair, sloughing of skin or in the urine. Lossess duringmenstruation 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 toblood 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 themuscles (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 theescape of haemoglobin from the corpascles to the plasma. Blood may be haemolysedin 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 theircytoplasm. 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) MonocytesAgain lymphocytes 3 types A) T – lymphocytes B) B- lymphocytes C) Natural killer cells(I) Granulocytes: These cells originate from stem cells (haemocytoblastas) in redbone marrow and go through several developmental stages befor entering blood, aprocess called granulopoiesis. They follow a common line of development throughmyeloblast 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 bothdyes.(A) Neutrophils: Neutrophil is about 10-12m in diameter. Most numerous in the adultblood, about 60-70%. The necleus is many-lobed; the number of lobes varies from 2to 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 thebody. Mainly microbes, and to remove waste material. They are attraced in largenumbers to any area of infection by chemical substances, released by damaged cells,called ‘Chemotaxins’. Neutrophils pass through the capillary walls in the infected areaby amoeboid movement. There after they ingest and kill the microbes by a processcalled “Phagocytoses”.(B) Eosinophils: Eosinophils is 10-12 m in diameter. Eosinophils are charecterised bytheir two-lobed. Nucleus they have significant proinflammatory and cytotoxic activityand play a role in the pathogenesis of various allergic, parasitic and neoplasticdisorders. The eosinophils are amoeboid but not phagocytic. Eosinophils is about 2-4%. The most common causes of eosinophilia in the world are allergic disorders suchas asthma, eczema and high fever. In developing contries parasitic infections arefrequently 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 basophilicstain. Basophils are the least numerous of the blood leucocytes. Basophils secretehistamine which causes vaso dilatation and increases the permeability of capillarywalls. Basophils and their tissue equivalent, most cells, have receptors for the protionof I g E. They play a central role in immediate hypersensitivity reaction. Basophils
    • is usually associated disorders Eg. Chronic myeloid leukaemia. However it may bereactive to a range of systemic diseases including inflametory bowel disease andhypothyroidism. Basophil count about – 0.5-1%.(2) A granular leukocytes (Agranulocytes): The type of leukocyte with no granulesin 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. Somecirculate in the blood and are actively motile and phagocytic, while others migrate intothe tissues where they develop into macrophage.The macrophage system, some timecalled the lymphoreticular system, consisits of fixed pahgocytic cells which multiplyin 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 receivingcortico steroid treatment. Monocytes count – 3.8%.Lymphocytes: Lymphocytes are developing from haemocytoblasts in red bonemarrow. Lymphocytes are associated with protection of the body against foreignmaterial. Lymphocytes are spread in the blood stream to lymphoid tissue else where inthe body where they are activated i.e. they become immunologically competent
    • which means they are able to respond to antigens (Foreign material). Lymphocytescount about 20-25%.The major types of lymphocytes are T-lymphocytes, B-lymphocytes and natural killercells. 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 cellsact directly against antigens in conjuction with phagocytes. The main T-lymphocytesare cytotoxic and are responsible for long-term protection against some viruses,bacteria, fungi, cancer cells, pollenfrom flowers and platns, some large moleculedrugs Eg. Pencillin. They are also responsible for the rejection of transplanted organsT.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 chemicalsubstances (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 byboth microbes and their toxins. B-Lymphocytes, which are responsible for humoralimmunity. These are five subclasses IgG, IgA. IgM, IgD and IgE. The antibodiespromote 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 ofmegakaryocytes in red bone marrow. The normal platelet count is between 2,50,000 to40,00,000/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 itsvessels. If it is drawn from the body, however, it thickness and forms a gel. Eventuallythe gel separates from the liquid. The red-coloured liquid called serum. The gel iscalled clot. The process of gel formation it called clotting or coagulation. Clottinginvolves 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 ofactivated 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 theintrinsic pathways blood clotting.
    • Extrinsic path way: The extrinsic pathway of blood clotting has fewer steps than theintrinsic 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 asthromboplastin or coagulation factor III, leaks into the blood from cells out side(extrinsic to) blood vessels and initiates the formation of prothrombinase. IF ismixture with of lipoproteins and phospholipids released from the surfaces of damagedcell. It activates clotting factor VII, which next combines with factor X, thusactivating it. Once factor is activated, it combines with factor V in the presence ofcalcium ions (Ca2+) to form the active enzyme prothrombinase. This completes theextrinsic pathway.Intrinsic pathway: The intrinsic pathway of blood clotting is more complex than theextrinsic pathway. And it occurs more slowly, usually requiring several minutes. IFendothelial cells (cells in the blood vessel) become roughened or damaged, bloodcame in contact with collagen in the surrounding basal lamina, in addition, trama toendothelial cells causes damage to blood platelets, resulting in the release ofphospholipids by the platelets. Contact with collagen activates clotting factor XII. Inturn, factor XII activates XI which activates factor IX. Activated factor VII (Fromextrinsic pathway) also can activate factor IX. Activated factor IX joins with the factorVIII and Platelets phospholipids to activate factor X. Once factor X is activated itcombines with factor V to form the active enzyme prothrombinase.Stage2: Once prothrombinase is formed, the common pathway follows. In the secondstage of blood clotting, prothrombinase and Ca2+ catalyze the conversion ofprothrombin to thrombin.Stage3: In the third stage, thrombin, the presence of Ca2+, converts fibrinogen, whichis soluble to loose fibrin threads, which are insoluble. Thrombin also activates factorXIII (fibrin stabilizer factor), which strengthen and stabilized the fibrin threads into asturdy 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 canact as antigens, are normal components of one person’s RBC plasma membrane thatcan trigger damaging antigen – antibody responses in other people. Based on thepresence 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 thatare present on the erythrocytes. Persons with type A blood have a Aantigens. Thosewith type B, B antigens: Those with type AB, both A and B antigens: In addition, theplasma of group ‘O’ blood contains antibodies to A, B and AB. Group A plasmacontains antibodies to B antigens and group B plasma contains antibodies to Aantigens. Group AB plasma has no antibodies to O, A, or B antigens. In bloodtransfusions cross-matching is necessary to prevent agglutination of donor red cells byantibodies in the plasma of the recipient because plasma of groups A, B and AB hasno antibodies to group O erythrocytes, people with group ‘O’ blood are called‘Universal doners’. Conversely, persons with AB blood are called Universalrecipients, because their plasma has no antibodies to the antigens of the other threegroups.In addition to the ABO blood grouping, there are Rh (Rhesus factor) – positive andRH Negative groups. An RH-Negative person can develop antibodies to Rh positivered blood cells if that person is exposed to Rh. Positive blood. For example, duringpregnancy a mother who is Rh negative can make antibodies for Rh-possitive cells inthe fetus is Rh positive (inherited for Rh positive). Rh-positive red cells from the fetuscan enter the maternal blood stream at the time of plancental separation and induceRh-positive antibodies in the mother plasm. The Rh-positive antibodies from themother can also reach the foetus via the placenta, and agglutionate and haemolyzefoetal red cells. This condition is known as Erythroblastosis foetalis, a haemolylicdisease 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 sweat glands. 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. Wills Biochemical Basis of Mecdicine. 13. Regional and Applied Human anatomy by Dr. B.D. Chaurasia.
    • NIDANA The word panchalakshana nidana indicates that there are five topics to discussunder 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 aeteologicalfactors in modern medicin. “Seti kartavyatako rogotpadaka Heturn nidanam” Means the factors, which plays an essential role in causing a disease vividhaahita ahara vihara which cause vyadhi by vitiating doshas and dhatus. Various factors are mentioned for the etiology of the disease. In the context ofPandu roga all factors responsible for aggravation of pitta are termed as specificnidanas. It can be stated that pitta prakopa nidanas cause the disease. The ahara andvihara 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 aggravateto pitta. Especially, amlarasa does kapha vilayana, pitta vardhana, rakta dooshana andsydhilya (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 turmincreases pitta, Tila is pittakara and ushna veerya. Ati teekshana ahara causes daha as it is of Agni boota predominance. Madhyadoes 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 increasedcatabolism, thus contributing to the cause of the disease. Panchakarma vaishamyavegavaroodha does vitiation especially to vata and thus cause disease pandu roga.Among all Panchakarma vyshamyas, Atiraktasravam during rakta mokshana is also acause 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 vitiatesvata 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 toPandu roga.Papakarma factors: (Sinful act) A person acquired Panduroga by sinful act according to the references fromVaidya chintamani i.e. one who steals things of Gods and Brahmanas, one who doesnot complete Agnistomadi karmas and one who kills a woman. Such persons acquirePandu with severe headache and with symptoms of kshaya. Such type of Pandu doesnot get cured within nine years. Thus the nidana of panu roga has been elaborately touched and discussedbecause it has been said that "Chikitsa is Nidana Parivarjanam"Nidana as mentioned in different classicsAhara (Diet) related factors: S.No. Description Charaka Susrutha Madhavakara Haritha Vagbhta 1 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 theintake of food may be more, the disease is aquired due to pitta Vardhaka ahara as wellas viharas. This imbalanced diet contains more fats, however deficiency of vitaminsand minerals leads to anaemia.
    • ETIOLOGICAL FACTORSAnaemia 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 marrow1. 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, spleenand 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 theintestine, due to infiltration into the blood stream.Ex. Malarial Parasite may cause Anaemia due to Haemolysis (Distruction of Redcells). Nematodes like Ascaris, Enterobiasis (Pin warm), Tape warms and Hook warmsare caused to Anaemia in human being especially in children during the first decade oflife.
    • In effects individuals at all socio-economic level especially children crouded livingconditions 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, andshed eggs, caused by the Symptoms like Anorexia, Indigesation, Abdominal pain andFullness of abdomin, and Diarrhoea occurs. The major manifestation of infection issubsequent 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 ROOPA According to susrutha, the sanchita and prakopita doshas are occumulated in aparticular stana it is termed as “Stana samshrayaavasta” a premonitory signs andsymptoms of manifestation of vyadhi. Those signs and symptoms which appearsearlier 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 observedby 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 diseasestart to occur. In other words, it is described as the early stage of any disease. It is thatstate of the disease, where Dosha – Dooshya Sammoorchana occurs, i.e. there beginsan 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 thefollowing days but not the detailed description of the predominant dosha. Viseshapoorva 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, PeetatwamPoorvaroopa – According to different acharyas :Sl Poorvaroopa Charaka Susrutha Vagbhata Hareeta1 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 ofthe classics, we can divide the above poorva roopas upon the doshic predominanceand 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 ofAnemia. Especially, these depend upon oxygen carrying capacity of the blood. Theseverity of the signs and symptoms depend upon the degree of anemia, independent ofits type. Lassitude and Fatigue, though are seen in the early stages of the disease, theseare seen in many other disease. Pallor of skin, mucous membranes, palms andconjunctivae are seen after some period and these in addition to above may give abetter picture of this disease. The complete picture of the disease shall be discussedunder 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
    • ROOPA This is the stage of a disease where the signs and symptoms of the disease aretotally manifested, this termed as fifth kriya. Kaala of ‘vyaktibhava’. When thedisease starts to take its stage forth kriyakala namely in the Stanasamshrayaavasthaor Poorvaroopavasta and when it is not treated the doshas get accumulated andmanifestiation into the diseased state – “ROOPA”. “Tadeva vyaktatam yatam rupa mityabidiyate” The poorva roopa which has attained vyakthavastha known as roopam. Thesymtpems are mainly due to sroto dushti of the respective Srothases. The main srotasinvolved in pandu roga is Rasavaha srota drushi. Hence, almost all of Rasavaha sroto dushti lakshanas can be observed in pandusymptomatology. These are Aruchi, Ashraddha, Agnimandya, Hrillasa, Arasagnatha,Gouravam, Tandra, Angamarda, Pandutwam, Jwara, Klaibhyam, Sada, Krishnagataand 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, andOjus 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 inbelow.Lakshanas of vataja pandu roga:S.No. Symptoms/sign Cha Su Va Ma Bha Ha1 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 rogaS.No. Symptoms/sign Cha Su Va Ma Bha Ha1 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 & KaphaS.No. Lakshanas of pandu Vataja Pittaja Kaphaja1 Varna of vit, mootra Krishna Peeta Sukla Nakha and Netra2 Jwara Present Present Present3 Shotha Present Absent Present4 Kamitwa Absent Seeta Ushna./katu5 Mukha ruchi Vairasya Katu Madhura6 Moorcha Absent Present Present7 Pureesha Little in quantity Bhinna Constipated8 Varna Aruna Peetha/haritha Swetha9 Bala Decreased Decreased10 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 theirrespective tables. However the clinical features shall differ as per the doshadhikyata. Hareeta mentioned that sannipataja pandu has the following lakshanas inaddition to above.Tandra Hrillasa Kshudarthata KasaAlasyam Shosha Moha JwaraSwayathu Vitbhada Trishna GlaniVamana PurushanayanaMadhava nidana added Arochaka and Haterndiya to above features.Mrit Bhakshanajanya Panduroga: The name Mritbhakshana janya pandu, as the name indicates, occurs due tointake of Mrittika (mud/pica). This geophagia vitiates all the three doshas. Butdepending upon the rasa of mud eaten, any of the three doshas vitiate, predominantly. Mrit generally contain ruksha guna in predominance. This makes the foodconsumed and the srotas, to dry. This leads to obstruction of srotas and even vitiatesrasa 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 ofthe blood. Their severity depends on the degree of anaemia and the pace of itsdevelopment. The Signs and Symptoms are listed below.S.No Symptoms Signs1 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 symptomsmentioned above since anaemia is caused by different etiological factors, their clinicalfeatures 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 manyinstances.INVESTIGATIONSBlood 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 ferritin 13. 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 excessiveurobilurubin for occult blood and melena.4. Bone marrow bipsy5. E.C.G.: ECG should also be done because, most of the signs overlap withcongestive cardiac failure and other valvular heart diseases.6. Endoscopy: sigmoidoscopy / proctoscopy / Gastroduodenoscopy7. IVP : Intravenous pylogram may be useful in haematuria is present.8. Jejunal biopsy9. Cr-51 labelled RBC infiltration. IRON DEFICIENCY ANEMIASAge Group: This type of anemia is mostly seen in children between ages of 6 monthsand 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 ageand it is almost universal during pregnancy.DIETARY HABITS: Vegetarians are more commonly affected with Iron Deficiencyanemias than non vegetarians. Consuption of white bread, polished white rice, whitesugar 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 andHemic 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 Rombergs 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 andduring pregnancy this deficiency can even lead to umbilical cord and neural canaldeficits.Dietary habits: Strict vegetarians (Veganism).Social Status: Poor people are more sufferers of anemia The above said Iron Deficiency anemia and megaloblastic anemias if untreatedlead to fatal Pernicious Anemia from severe form of blood disease, marked byprogressive decrease in RBC, muscular wekness, GI & neural disturbancesAge - 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.
    • SAMPRAPTI Samprapti is the stage wise manifestation of the disease. The disease process isstarts with nidana and then passes through Sanchaya, prakopa, prasara,Stanasamsraya and Finally manifestation of Vyaktavastha, i.e. manifestation ofpandu. This complete disease process is called as samprapti. In other wordsSamprapti 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 particularvyadi. 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 ofthese nidnans pittavridhi takes place. Physiologically the formation of acchapitta,occurs in Grahani during ahara parinama. But due to katu, amla, lavana, ushna aharaand other causes mentioned earlier, vitiation of pitta takes place. Since Pachaka pittais situated in Grahani, the vitiated pitta affects the Agni. The drawatwa in thisvidagdha 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 andKittabha by samana vayu and the saarabhaga is taken to hridaya. But due to vidagdhapitta, pachana does not occur properly leading to dooshita annarasa. The annarasa istaken by samanavayu to hridaya and transforms it into rasadhatu. The viharas likevyayama, vyavaya etc cause vitiation of vyanavayu. The viitiated vyana vayu alongwith pitta - dooshita rasadhatu circulates throughout the body through dasa dhamanisthat emerge from hridaya. The pitta dooshita rasa dhatu flows into the next dhatu for
    • its nourishment malformed rasa dhatu due to pittavidagdata, destructs theraktadhatu poshakamsas and attains pandu roga, which will not be in a position tonurish dhatus. Finally rasadhatu lodges in the space between twak and mamsa. Then byvitiating the kapha, vata, rakta, twak, and mamsa, it produces pandu, haritha andharidra varnas, or various other discoloration of the skin. Of these colours, pandu isseen predominantly. The formation of all the other dhatus is also impaired. As aresults of this, the formation of next dhatu i.e. raktadhatu is effected both qualitativelyand quantitatively. Even the essence which comes out from each dhatu also reduces inits quantity. As the essence of all dhatus is ojus, its kshaya lakshanas can also beobserved on progression of the diseases. In pandu the rasa dhatu dushti and there by its kshaya takes place. Hence in thefirst stage of the disease, rasadhatu kshaya lakshanas are predominantly seen. Thoseare 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. Thenidanas which vitiate ranjaka pitta and rakta directly causes the kshaya of these twoand / or the qualities of these two are also altered. These are responsible for thedisease pandu. Hence ranjaka pitta and rakta kshaya lakshanas are observed in thedisease. 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 themadhura rasa mrit. Generally mrit contains ruksha guna. Hence the consumption of mrit mainlyvitiates vata. Mrit does not contain any dhatu poshka amshas. It obstructs all thesrothasas 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. Thisimpairs even the formation of ojus also. The resultant manifestations are loss ofenergy of indriyas and tejus. Finally the disease sets in with bala, varna, andagninashana, swelling of akshi, ganda, akshikoota, pada, nabhi, medra, krimikosta,and atisara - as well as kapha - rakta yukta pureesha occurs. Thus samprapti of panduroga 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 LAKSHANAS It is very essential to decide the sadhya and asadhya of any disease beforeattempting to treat it. As a general rule, the disease without any upadravas, or aristalakshanas, which is newly manifested, which has less number of lakshanas and inwhich only one dosha is involved is said sukhasadhya. Asadhya denotes the badprognosis of the disease. Asadhaya lakshanas are two types – Yapya andPratyakhyeya. Yapya is the term used when the disease is incurable and the patientsurvives 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 ofchronic in nature, the disease is said to be pratyakhyeya. It has been mentioned thatthe physician should leave the patient untreated, if the below mentioned asadhyalakshanas 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 patientsin the study. If the patient develops the above clinical features, then the physicianshould 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 LAKSHNASUpadravas: Any vyadhi or clinical features appearing on the later stage of a maindisease due to improper management are called as upadravas of the disease. Whenupadravas occurred the disease becomes very difficult to treat. It denotes that thedisease 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. Thedosha involvement in the upadravas may be equivalent to the main disease (or) maynot be.Arishta lakshanas:Arista lakshanas are Asanna marana lakshanas. These are the clinical features thatappear 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 physicianshould 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 KRAMA The chikistsa karma means. Stage – wise treatment program of the disease. Ingeneral, the three principles of treatment mentioned in ayurveda areDiavavyapasraya, Yuktivyapassraya, and Satwavajaya. Daivavyaaprasrayachikista mainly depends on praying God, doing yagnas and yagas, doing good deedsetc Yuktivyapasraya chikitsa of pandu roga includes the following principles. 1. Nidana parivarjana 2. Snehana chikitsa 3. Shodhana chikitsa 4. Samana chikitsa1. 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, Teekshnaaharas, 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, butswedana chikitsa is contra indicated in case of pandu roga, because it is pittapradhanavyadhi. The patients of pandu have dhatu kshayam which is due to impropernourishment of rasadi dhatus. As a result, rukshatwa occurs in the body. This is anecessary treatment before any shodhana karma. Shehana does srotho mardhava andhelps the doshas come out freely when sodhana karma is done. Snehapana is evenmore important in case of mrit bhakshana janya pandu, because the mrit causesrukshatwa in the srothas and causes obstruction in srotas. Sneha karma is indicatedbefore and after shodhana chikitsa in Mrit bhakshana janya pandu. Since Pandu
    • roga is pitta pradhana disease, the following tiktaghritas are mentioned for snehakarma. 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 ghritam3. Shodhana karma: Charaka, Vagbhata and others recommended strong emesis and purgation aftergiving oleation therapy. Shodhana karma pulls out the doshas with their roots and prevents thereoccurrence of the disease. The shodhanakarma indicated in pandu are Urdhwashodhanam (Vamana) and Adhah shodhanam (verechana) A) Urdhwa shodhanam (vamana): Charaka stated that teekshana guna yuktavamana oushadhas are indicated in pandu roga. Though susrutha contraindicatedvamana in pandu roga. Dalhana advocated Mridu vamana, when Rutu, Desha, Kalaare 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 MritbhakshanajanyaCha Snigdha Tikta and Katu ruksha Tridoshahara Strong samshodana & Madhu sheeta and Ushna of GITSu Snigdha Tikta and Katu ruksha Tridoshahara - & Madhu sheeta and ushnaVag Durgs Drugs of More Tridoshahara Strong purification Possing bitter taste pungent dry therapy sneha and cold and hot potensive potencyBR Medicines Tikta and Katu ruksha Tridoshahara Strong purification with gruta sheeta and ushna therapy base medicines medicinesBV Mediciens Tikta and Katu ruksha, Tridoshahara Strong purification with gruta sheeta and ushna therapy base medicines medicinesYR 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 sheetalam Slaishmike 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 guna dravyas. l Sannipathaja pandugaroga is to be treated with mishrita dravyas.In shamana chikitsa, the following drugs are mentioned : Single drugs:Herbal drugs Mineral drugsPathy Loha bhasma / choornaAmalaki Mandoora bhasmaYashtimadhu Kaseesa bhasmaDraksha Abhraka bhasmaBrihat panchamoolas Swarna maksheka bhasmaGuda SilajitTila Pravala bhasmaHaridra Mukta bhasmaShunti Sankha bhasmaPippali Jasada bhasmaBhringaraja Kantha bhasmaKumari Tamra bhasmaPunarnava
    • 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 prashavalehyaAsava / Arishtas 1. Goudarishta 2. Beejakarishta 3. Dhatryarishta 4. Lohasava 5. Ayaskriti 6. Bringarajasavam 7. Kumari asavam 8. PunarnavasavamAnupaana:The substance that is consumed along with or after the intake of oushadha dravya isAnupana. This may be either solid or liquid in nature. Anupaana should fulfill thefollowing 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 variousauthors. 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 bloodwith 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 APATHYAS The knowledge of Pathya and Apathya is essential in treating the disease. Allthe nidanas mentioned in nidana aspect are to be strictly considered as apathyas andare to be avoided. Those aharas and viharas, which are against the nidana as well as the disease arecalled ‘Pathyas’. In contrary, the aggregating factors of the disease are called‘Apathyas’.Pathya (Upasaya): Food that are capable of causing agnideepana should form asimportant 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 fruitsApathyas: 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 thenidanas, 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 DRUG The drug selected for present clinical study is "Bhaskara Lavana Churnam". Itsanupana is "TAKRA". The administration of Bhaskara Lavana Churnam is advised inthe condition of panduroga. The drug has been selected to evaluate its efficacy inpandu roga. The reference to the present clinical study is taken from the Baishajyaratnavali. "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 ofPandu, Pleehavyadhi, Krimi, Ajeerna, Aruchi, Arshas, Shoda, Amadosa. The drug hasbeen selected to evaluate its efficacy in pandu. The preparation is non contraversial and the ingredients are easily available. Thisformulation is easy to prepare and free from toxic effect. The compound herbo mineral drug Bhaskara lavana churnam consists ofingredients Samudra lavana, savarcha lavana, saindava lavana, Bida lavana, Dadimabeeja, Pippali, Pippalimula, Dhanyaka, Kalajeera, Teja patra, Talisa patra,Nagakesara, Amla vetasa, Kalimareecha, Swetha jeera, Sunti, Twak, Ela. So thisBhaskara lavana churnam mainly Tridoshahara, rasayana, Deepana, Pachana, Hridya,Balya, Ruchya properties. It helps in pitta dosha samana, Deepaneeya and raktavardhaka. It has the direct action on Amasaya, Yakrit and Ranjaka pitta. Agni vikriti is another importent clinical condition of pandu roga. Samagni is anessential factor for the proper digestion and assimilation of ahara rasa, with themandagni avastha samyak ahara rasa formation will not take place. According tocharaka rakta poshakamsas are present in rasadhatu and owing to improper rasaformation, proper development of raktadhatu is not possible, and the above conditionresults 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 shamanaAgni Deepana, pachana and raktavardhakas, therefore helps in the production ofintrinsic factor and assimilation of extrinsic factor. It also avoid the accumulation byvirtue of its purgation property. The pandu roga is pitta prakopaka vyadhi. In general the salts, main the saindavalavana being seetagunam, Snigdhaguna, Avidhahi, Madura vipaka and Tridoshahara.It acts pitta samaka. All salts are accepted as good preservatives which help inreataining the potency of the prepared medicine for longer periods. The pippali is explained as Rasayana in Ayurveda, addition of pippalli andlavana churnas to the ingredients may help in faster absorption of the drug. The Dadima, pippali, pappli mula, Dhanyaka, jeeraka, Tejo pathra and Twakcontains the property of krimigna. So are responsible for the elimination of worminfestation, 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 Raktadhatu dusti. So this may help to increase the taste. The Shunti, Jeeraka, Dhanyaka, contains grahi guna, that is responsible for theactive absorption of lohasma in ahara and oushadha. The Balya property of swethajeeraka assists in alleviating the dhatukshya andojokshaya, present in Pandu Roga. The statement "Samanyam Ekatwa karam" mentioned in ayurvedic classics isjustified 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 theAmlavetasa, 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 lumpsin the mines in Beluchistan, sindh and upper Punjab. It is natural sodium-potassiumchloride. 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 sodiumchloride in impure form.
    • SAUVARCALA LAVANA Synonyms: 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 artificialproduct, prepared by mixing saindhava, haritaki, amalaki, and sarjakshara (sodiumcarbonate), boiling these in water tilt evaporation is complete. Then the mess isbroken to pieces and sold.
    • SHUNTISynonyms : Viswabheshaja, Nagara, Ushna, Katubadra,Sanskrit : NagaraTelugu : SuntiHindi : SontiEnglish : Dry ZingerLatin Name : Zingiber officinaleFamily : ZingiberaceaeGana : Pippalyadi, Triptighna, Deepaniya, Vachadi, Arshoghna, Sthanya Shodana, Trishna Nigrahana, Sheeta prasamana, Shodhaprashamana, Pachaneeya, Haritakyadi vargaRasa : KatuGuna : Laghu, SnigdhaVeerya : UshnaVipaka : MadhuraParts used : RhizomeKarma : 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, RaktapuspaBotanical name punica granatumFamily punicaceaeTelugu Danimma kayaHindi AnarEnglish pomegrantiMalayalam matalamTamil maduliGanas According Caraka – hridya, chardinigrahana Susruta – Parusakadi Vagbhata - ParusakadiTypes According to Kaiyadevara & Bhavamisra – 3 vareities of dadima 1. Svadvamla 2. madhura 3. amlaRasa Kasaya. Madhura, amlaGuna Laghu, snigdhaVirya UshnaVipaka Madhura / AmlaKarma Tridoshahara, Hridya, Sukrala, Grahi,Dosage Fruits juice 20-50ml. decoction 40-80ml. bark powder 3- 5gPart used FruitChemical compositon Fruit peels – Kannins, Punicatin. Seeds, Estrone, Danicic Danicic acid Stem – Malvidin, Pentosa, Ilucosides, Tannin Ca, Mg, Na, Iron, Tamram V B1 B2.
    • PIPPALIynonyms: Kana, Krsna, Kola, Capala, Triksna Tandula, Magadhi, Vaidehi, Usana, Soundi.Botanial name: Piper longum linnFamily: PiperaceaeHindi Pipal ,English Long pepperTelugu PippalluTamil TippiliBengali PipulMalayam TippaliGanas: According to Susrutha Pippalyadi, Urdhvabhagahara, Triyushana (Trikatu) Amalakayadi, Sirovirecana. According to Vagbhata Pippalyadi ( A.S)Past Used : Fruit, RootRasa Katu,Guna Laghu, Snigdha TiskhanaVirya Ushna,Vipaka MadhuraKarma: 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 MULASynonyms Kana, Krisna, Kola, Capala, Tiksnatandula, Magadhi, Vaidehi, Sauna, SoundiBotanical name Piper longumFamily PiperaceaeTelugu PippalluHindi PippalaEnglish Long piperTamil TippiliGanas According to Kasahara, Hikkanigrahana, Seroverechana, Vamana, Triptigna, Deepaniya, Shoola prasamana According to susrutha – pippalyadigana According to vagbhata – pippalyadiTypes According to susrutha & vagbhata have defined 2 varietes pippali, Gajapippali According to Rajanighantu – provides 4 varieties of pippali 1. pippali 2. gaja pippali 3. simhapippale 4. VanapippaleGunas Text Rasa Guna Veerya Vipaka Charaka Katu ushna Bhava Katu snigdha Anushna Madhura prakasa laghu Dhanvantari Katu snigdha ushna Madhura Nighantu laghu Kaiyyadeva Katu snigdha Anushna Madhura Nighantu laghuKarma Udara, pliharoga, jwara, kusta, prameha, Gulma, Arsas, Sula, amavataDosage: Powder ½ -1 gramsPart used: Fruit, rootChemical compositon Essential oil, and sesquiterphon, caryophyllene (mainly),piperine, piplartine piper longumine, sesamin, B-site sterol, Resin, Olatile oil.
    • DHANYAKASynonyms Kustumburo, Chatra, Vittunnaka, DhanyakaBotanical name Corundum satirumFamily UmbellifereHindi DhaniyaTelugu Dhaniyalu English – Coriander seedsGanas According to Caraka – Trsnaprasamana, Sulaprasanama According to Susrutha – Guduchyadi According to Vaghata - GuduchyadiRasa Kasaya, tikta,Guna Laghu, snigdhaVeerya UshnaVipaka MadhuraKarma Tridosha hara, Deepana, Paachana, GrahiIndications Jwara, Daha, Trusna, Chardi, Kasa, Swasa, … arsasDosage Fruit powdar 3-6 gms, cold infusion 20-30mlPart used Fruit, whole plantChemical compositon Coriandrinol (glucoside) carotene cugenol, bergapten.
    • TEJO PATRASynonyms Tumburu, tejasvini, tejovati, vanaja, sourabhaBotanical name Zanthozylum ilatumFamily RutaceaeHindi TejabalaEnglish Toothache treeBengali Nepali dhanaGanas According to Caraka Sirovircchana, katu skandhaRasa KatuGuna Laghu, ruksaVirya UsnaVipaka KatuKarma Kapha – Vata hara, Kanthya, Dipana, PacanaIndications Hrdroga, Mukha roga, Dantaroga, Kantha roga, Hikka, Agnimandya, Arsas, Svasa kasa, Amavata, Apatantraka, UdaraChemical compositon Bark – herberine, xanthoplanine Fruit – arginine, histidine, thujene Root - spilanthol
    • TALISA PARTRISynonyms: Dhatripatra, patradhya, sukodaraBotanical name abes webbianaFamily pinaceaeTelugu & Tamil TalisapatriHindi & Bengali TallispatraEnglish Indian silverGanas: According to susruta -sirovirecanaTypes : According to Yadaviji trikamjit quoted 3 varieties (1) T. baccata (2) A. webbiana (3) R. lepidotumRasa Tikta, maduraGuna Laghu, tiksnaVeerya UsnaVipaka KatuKarma: Kapha, Vatahara, Hridya, DipanaIndications: Svasa, Kasa, Mukharoga, Ksaya, Chardi, Aruchi, Agnimandya, Gulma, Raktapitta, HikkaChemical compositon: Abesin, n-triacontanol, B.Sitosterd, betuloside, Riboflavonoid, betuloside
    • NAGAKESARASynonyms: Ahipuspa, loha. Kanakahva, kancanahvaya, kinijilkam, kesaram, campeyam, natam, nagam, naga kinjilkam. Nagapuspam, naga renuka, pinjaram, phani pannagam, rukmam, suvarnam hemapushpam.Botanical name Mescea ferreaFamily GuttiferaeTelugu Naga kesaraluHindi Iron wood of assamEnglish NaghasKannada KanchanaGanas: 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 vargaTypes: 1. Mesua ferrea 2. ochro carpus longitolasRasa Kasaya, tiktaGuna Ruksha, Tikta, laghuVirya usna/anusnaVipaka katuKarma: Kapha pittahara,. Pramathi, Grahi, Pachana, Visahara, sothahara, kandughna, kusthaghnaIndications: Raktarsas, Raktatisara, Raktapradara, Kusta, Visarpa, Jvara, Chardi, Vasti vikara, Vata rakta, Sopha, Vataroga, Siro roga, Trsna, Visa roga, KanduDosage: Powder of stamens 1-3g orallyPart used: StamensChemical compositon Squalene, cycloartenol, campesterol, stigmasterol, And bitosterol
    • MAREECHASynonyms : Mareecha, ushana, Vellaja, Krishna, DharmapattanaSanskrit : MareechamTelugu : MiriyaluHindi : Kalimirch, mirchEnglish : Black peperLatin Name : Piper nigrumFamily : PiperaceaeGana : Deepaniya, Shoola prasamana, Krimighna (Charaka); Pippalyadi, Tryushana (Susrutha)Rasa : KatuGuna : Laghu, Teekshna, Guru (Ardra)Veerya : UshnaVipaka : Katu Madhura (Ardra)Parts used : FruitKarma : Kaphavatahara, Deepana, AvishyaIndications : 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 JIRAKASynonyms Ajaji, kana, jarana, dirgha jirakaBotanical name cuminum cyminumFamily umbelliferaeTelugu JilakarraHindi Safed jeeraEnglish Cuminum seedsMarathi JircinKannada JirigeGanas: Caraka – Sulaprasamana Susruta – pippalyadi Vagbhata - pippalyadiTypes: 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 KatuGuna Laghu, ruksaVeerya UsnaVipaka KatuKarma: 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 rogaDosage: Fruit powder 3-6gPart used: FruitsChemical compositon: cuminin, isoimperatorin, cuminaldehyde, P-cymene, diacyl glycerol, imperatorin) paspharus, calcium, iron. Vit A.C. etc. …
    • KRISHNA JIRAKASynonyms: Udgarasodhana, sugandhaBotanical name Carum carviFamily UmbelliferaeTelugu NallajilakarraHindi SyahajiraEnglish Black carawayTypes Certain nighantu works described sexvareiteis 1. Sveta 2. Pita 3. Krsna 4. Suksma 5. Sthula 6. VanyajeerakasRasa KatuGuna RuksaVeerya UsnaVipaka KatuIndications Jvara, Chardi, Atisara, Gulma, Adhmana, AjeernaDose Fruit powder 1-3 grmsPart used FruitChemical compositon Essential oil, tricylo glycerols sterols, petroselinic acid, essential oil – carone
    • CHOTI ELASynonyms Korangi, Dravidi,Tuttha, Triputa, Trtisthula Ela – Bhadra ElaBotanical name Electtaria cardamomumFamily ScitaminaeTelugu Chinna elakulesHindi ChotiilaychiEnglish Lesser cardamomTamil YelakkaKannada ElakkiGanas 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, MadhuraGuna Laghu, ruksaVeerya SitaVipaka KatuKarma Kapha – vatahara, hrdya, sukra nasaka, deepana, pachanaIndications Hridroga, svasa, kasa, mutrakricchra, chardi, sirahsula, Arsas.Dosa Powder 0.5-1 gPart used SeedsChemical compositon Camphor citral, terpeneols, cymene, heptane sitosterol
    • TWAKBotanical Name Cinnamomum Zeylanica BlumeFamily LauraceaeHindi DalchiniEnglish CinnamonTelugu Lavanga pattaTamil IlayangamBengali DaruchiniGujarati TajaSynonyms: Utkata, tanutvak, darusita, varanga, svadvi, tvak, Patta, bhrngam, kavaca, sakala, saihala , latapatra, ramapriyaGanas According to Susruta-eladi According to Vagbhata Eladi, trijatakaRasa Katu,Tikta Madhura,Guna Laghu, Ruksha, Tiksna,Veerya UshnaVipaka KatuKarma Vata pittahara, Sukrala, Balya, Vatarsas, GrahiIndications Kandu, Amajirna, Aruchi, Krimi, HridrogaPart 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, ChallaHindi : Chancha, MattaEnglish : Butter milkRasa : Madhura, Amla, KashayaGuna : Laghu, Rooksha, Grahi, Vikasi, SaraVeerya : UshnaVipaka : MadhuraKarma : On dhoshas: TridoshaharamIndications : 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 basisof preparation of Takra it is of 4 types (Dhanvantari-Nighantu and Susrutha) and 5types (Bhava Prakasha). This Takra is one of the type among these.Details: According to Bhava Prakasha1. Gholam - By churning curd without water2. 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 theTakra preparation, as it can be prepared by squimming the curd by adding Halfquantity 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 andcontains proteins as like as milk, because this is free from butter. Butter milk containslacto bacilie ie., useful bacteria, which helps in the modification of milk to curd. Thereis change in the action also; milk can act as mild laxative, butter milk acts in reverseway, which is helpful for diarrhiea, as we are saying in the society.
    • MODE OF PREPARATION The preparation of Bhaskara Lavana Churna was prepared as follows accordingto 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. Atfirst, the all drugs were individually powdered finally and then mixed together in thequantities 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, andnutritional deficiency anemias.
    • MATERIALS AND METHODS The materials required a clinical study on the effect of "Bhaskara lavanaChoorna" in the management of Pandu roga are 1. Patients 2. Parameters 3. Drug1. 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 beenelicited about rogi and roga pareeksha are noted in the proforma of special case sheetof 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. PalpitationExclusion of criteria: 1. Pateints suffers with cardiac diseases 2. Patients who are below 6 grams of haemoglobin 3. Hemorrhagic disorders Eg: Hemorroids2. Parameters: The parameters that are used in assessing the results can be divided into two categories. a. Subjective parameters b. Objective parametersa. Subjective parameters: The following have been taken as subjective parameters. i. Relief of clinical signs and symptoms ii. Appearance of Rakta saara lakshanasb. Objective Parameters: The following have been taken as objective parameters.
    • i. Hemoglobin Percentage ii. Red blood cells count3. 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 shownby 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 andbars. These are presented in diagrams, so that records could be prepared properly. Thetables showing information regarding sex incidnece, mentioned in the chapter ofobservation and results.
    • OBSERVATIONS Thirty patients of Pandu attending the Postgraduate Kayachikitsa, department ofGovernment Ayurvedic Hospital, Erragadda, Hyderabad are randomly selected forthis 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 thetreatment are recorded. The condition of the patients is reviewed after every 15 and 45days of treatment. It is continued up to a duration of 45 days and the observationswere 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 3.33Out of thirty cases 25 cases were females, 4 cases were male and 1 malechildren were seen. No. of Patients 3.3% 13.33% Male Female Children 83.33%
    • Table 2. According to Age: S.No. Age group No. of male No. of female Total Percentage in 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 13.3330 patients were classified according to the ages as shown in table 2.Maximum caseswas seen in 31-40 year age group. 9 8 7 6 5 M a le 4 F e m a le 3 2 1 0 0-1 0 1 1-2 0 2 1-3 0 3 1 -4 0 4 1 -5 0 Age in YearsTable: 3 According to Diet: S.No. Diet No. of male No. of female Total Percentage patients patients 1 Vegetarian 2 11 13 63.33 2 Mixed 3 14 17 36.66In the present study the vegetarians are 63.33%, ( 13 out of 30) and mixed diet were seen 36.66% (17 out of 30). 14 12 10 8 M a le F e m a le 6 4Table 4: According to Economical status: 2 0 V e g e ta ria n M ix e d Type of diet
    • Table 4: Accoridng to Economical Status :S.No. Economical No. of male No. of female Total Percentage patients patients1 Poor 4 15 19 63.32 Middle 1 8 9 303 Rich 0 2 2 6.66 The patients were observed as per socio-economical status based on theirmonthly income. Out of 30 cases 19 casses were poor, 9 cases were middle classes, 2cases were seen rich.Table 5: According to Occupation:S.No. Occupation No. of male No. of female Total Percentage patients patients1 Labour 3 15 18 602 Student 1 6 7 23.333 Sedentary 1 4 5 16.33 Out of 30 cases, 18 casses were labour, 7 cases were Student and 5 sedentarycases were seen.Table 6: According to Prakriti:S.No. Prikriti No. of male No. of female Total Percentage patients patients1 Vata 2 6 8 26.662 Pitta 1 5 6 203 Kapha 2 14 16 53.33 In the present study 16 casses were Kapha predominent prakriti, 6 casses werePitta 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 Percentage1 Pandutwam 30 28 93.332 Sweta nakhata 30 25 83.333 Agni nasanam 30 30 1004 Aruchi 24 21 87.55 Angamardha 24 18 756 Kapha praseka 24 20 83.337 Brama 10 5 508 Jwara 15 13 86.669 Pindiko dweshta 20 14 77.7710 Tandra 20 16 8011 Alasya 20 16 8012 Gowravam 25 22 8813 Akshikoota sodha 4 2 5014 Krimi kosta 4 2 5015 Daha 13 10 33.3316 Prabha heena 20 14 7017 Swayathu 5 3 6018 Palpitation 20 13 68.42In the present study symtpoms and signs seen before and after the treatment
    • MASTER CHART, SHOWING DATA IN RELATION TO PANDU ROGA After treatment Before treatmentS. Name Age S Reg Diet Econo- Occupati Prakrati 0 days 21 days 45 days ResultNo e No. mical on x Status Hb RBC Hb RBC Hb RBC1 Rajyalaksh 30 F 11185 Mixed Middle Sedentar Pitta pre. 7.0 3.2 8.2 3.8 9.4 3.2 Avara mi y2 Vijayalaks 35 F 11117 Vegetaria Poor Student Vata pre. 6.3 2.8 7.8 3.1 8.8 3.1 Avara hmi n3 Vijaya 40 F 21492 Mixed Poor Student Kapha 10.5 3.4 12.1 3.1 13.1 5.1 Pravara Marry pre.4. Madhavi 25 F 11186 Mixed Middle Labour Kapha pre. 8.0 4.2 9.2 4.4 11.8 3.8 Madhya ma5. Mahaboob 40 M 14667 Mixed Poor Labour Kapha pre. 11.5 3.2 12.3 4.9 13.2 4.8 Pravara vali6 Eswaram 40 F 19184 Vegetaria Poor Labour Kapha pre. 10.2 3.1 11.6 3.3 13.3 3.5 Pravara ma n7 Ramadevi 34 F 21497 Mixed Poor Labour Kapha pre. 9.0 4.2 9.4 4.4 11.6 4.5 Madhya ma8 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 Poor Sedentar Kapha pre. 9.8 3.4 10.9 4.3 13.1 4.5 Pravara n y10 Asiyabegu 27 F 5553 Mixed Middle Labour Vata pre. 8.0 2.9 8.8 3.6 9.8 3.8 Avara m11 Lakshmi 45 F 11582 Vegetaria Poor Labour Kapha pre. 10.0 4.1 9.8 4.7 11.8 4.3 Madhya n ma12 Tulasi 45 F 11118 Mixed Poor Labour Vata pre. 10.2 3.8 12.2 3.3 13.0 4.6 Pravara13 Sabeyabe 17 F 11135 Vegetaria Middle Labour Kapha pre. 10.0 3.2 11.6 3.2 13.2 3.5 Pravara gum n14 Sudershan 6 M 11272 Vegetaria Poor Sedentar Vata pre. 7.0 3.2 9.2 4.3 10.0 3.5 Avara n y15 Sarada 24 F 14287 Vegetaria Poor Sedentar Kapha pre. 8.5 3.8 9.4 3.9 10.8 3.8 Madhya n y ma16 Kirankum 22 M 8505 Mixed Middle Student Pitta pre. 10.5 3.4 12.6 4.6 14.0 5.1 Pravara ar17 Sunitha 23 F 8936 Vegetaria Poor Student Kapha pre. 10.5 3.4 11.6 3.1 12.8 4.8 Pravara n18 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 42 F 17771 Vegetaria Poor Labour Pitta pre. 11.0 3.2 12.8 3.6 13.1 4.8 Pravara um n21 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 Poor Sedentar Vata pre. 10.5 3.3 10.9 3.7 13.6 4.8 Pravara n y23 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 Poor Labour Vata pre. 9.5 3.9 11.8 3.1 12.9 4.5 Madhya n ma25 Anitha 30 F 22646 Vegetaria Middle Labour Vata pre. 11.0 3.8 12.8 3.3 12.9 3.5 Pravara n26 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 Poor Labour Kapha pre. 8.2 3.1 10.3 4.0 12.9 4.8 Pravara n30 Yallamaia 40 M 24705 Vegetaria Poor Labour Kapha pre. 10.1 3.9 11.4 3.6 11.8 4.2 Madhya h n ma Final Result: After the completion of 45 days of treatment Pravara 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 treatmentHb levels 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 12.1-13in gramsMales 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 0In the present study the haemoglobin levels ranged from 6 to11.5 gms/dlbefore the treatment. 8 8 8 7 6 5 5 Males 4 Females 3 2 2 2 2 1 1 1 1 0 0 0 0 6.1-7 7.1-8 8.1-9 9.1-10 10.1-11 11.1-12 Hb levels (gms) Table 9 : Heamoglobin levels after 21days of treatmentHb levels 6.1-7 7.1-8 8.1-9 9.1-10 10.1-11 11.1-12 12.1-13 13.1-14in gramsMales 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 0Hb levels showed gradually increased with in 21days from the starting day of treatment.6 65 5 5 54 3 Males3 Females2 2 21 1 10 0 0 0
    • Table 10 : Heamoglobin levels after 45 days of treatment.Hb levels 8.1-9 9.1-10 10.1-11 11.1-12 12.1-13 13.1-14 14.1-15in grams 7.1-8 Hb levels (gms)Males 0 8.1-9 1 9.1-10 0 10.1-11 1 11.1-12 1 2 12.1-13 0 109Females 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 0Hb levels achieved to maximum levels with in 45 days of treatment. 8 8 8 7 6 5 4 Males 4 3 Females 3 2 2 1 1 1 1 1 1 0 0 0 8.1-9 9.1-10 10.1-11 11.1-12 12.1-13 13.1-14 Hb levels (gms)Table 11: RBC levels before treatment.RBC levels in 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 5.1-5.5mill/cummMale 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.12 1110 8 7 Male 6 Female 4 4 3 3 2 2 110 0 0 0 0 0 RBC levels (millions/cumm)
    • 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/cummMale 1 1 1 2 0 0Female 9 10 4 2 0 0Total 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. 10 9 8 7 6 5 M a le F e m a le 4 3 2 1 0 3 . 1 -3 . 5 3 . 6 -4 .0 4 . 1 -4 . 5 4 . 5 -5 .0 5 .1 -5 . 5 RBC levels (millions/cumm)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/cummMale 0 0 2 3 1 0Female 6 5 3 9 1 0Total 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. 9 8 7 6 5 M a le 4 F e m a le 3 2 1 0 3 . 1 -3 . 5 3 . 6 -4 . 0 4 . 1 -4 . 5 4 . 5 -5 . 0 5 . 1 -5 . 5
    • RESULTS The results of the treatment of assessed periodically after 21 and 45 days till the RBC levels (millions/cumm)completion of the duration i.e.45days. the results are tabulated according to the signsand 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 Avarage 1 Male 2 2 0 2 Female 16 5 4 3 Children 0 0 1 The present study comprises 13.33% of adult males (4out of 30), 83.33% ofadult females (25 out of 30) and 3.33% (1out of 30) of male children. Out of these6.7% (2out of 5) among males, 60% (16 out of 25) adult females got best result.
    • 16 16141210 Male 8 Female 6 Children 5 4 4 2 2 2 1 0 0 0 0 Pravara Madhyama Avara RESPONSE BASED ON SEX Table No.2: Responce based on Age. 112s.no. Age Pravara Madhyama Avara (years) Male Female Male Female 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 youngest being 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 patients achieved best results followed by 2 madyama and one avara patients. 16 out of 25 adults females got best results, followed by 5 madhyama and 4 avara patients. 7 7 6 6 5 Pravara 4 Madhyama 3 3 3 Avara 2 22 22 1 1 1 1 0 00 00 0-10 11-20 21-30 31-40 41-50 RESPONSE BASED ON AGE
    • Table.3: Response based on Diet. s.no Type Pravara Madhyama Avara Diet Male Female Male Female Male Female 1 Vegitarion 0 7 2 1 1 1 2 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 of vegetarians 23.3% (7out of 30).14 131210 8 7 Vegitarion 6 Mixed 4 3 3 2 2 2 0 Pravara Madhyama Avara RESPONSE BASED ON DIET 113 Table No.4: Response based on Economic status Economic Pravara Madhyama Avara Total Status 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 2 In 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 (15 out of 30) among poor. Table No. 5: Response based on symptoms/signs S.No. Symptoms/Signs No.of Improved Partially Not cases 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 Brama 10 4 1 58 Jwara 15 10 3 29 Pindikodwesta 18 12 2 210 Tandra 20 14 2 411 Alasya 20 15 1 212 Gowravam 25 20 2 313 Akshikoota sodha 4 6 2 214 Krimikosta 4 0 2 215 Daha 30 15 10 516 Prabhaheena 20 10 4 617 Swayatha 5 3 1 118 Palpitaion 19 11 2 5 In the present study, pandutwa is an important symptoms that got considerabaleimprovement. 25 out of 30 pateints showed best results with complete relief, 4 withpartial improvement and 1 case showed little response towards treatment. Otherimportant symptoms such as agnimandhya, aruchi, Gowravam, and kaphapraseekamalso showed greater response to the treatment. The list of sign and symptoms beforethe treatment and after the treatment is tabulated above.Table No.6: Hemoglobin levels before treatmentHb levels Males Females Total Percentage %Pravara 0 0 0 0Madhyama 4 9 13 43.33Avara 1 16 17 56.66 In the present study, the hemoglobin levels ranged from 6 to 11.5 grams/dlbefore the treatment. Patients with very poor hemoglobin levels are 56.66% andpatients with average anemia are 43.33%. 16 14 12 10 M a le 8 F e m a le 6 4 2 0
    • 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 startingday of treatment. The poor haemoglobin patients before the treatment decreased from56.66% to 33.3%.Table.8: Hemoglobin levels after 45 days of treatment. Hb levels in Males Females Total Percentage% gms Pravara 2 16 18 60.00 Madhyama 2 5 7 23.33 Avara 1 4 5 16.66Hemoglobin levels achived to maximum levels with in 45 days of treatment.60% of thepatents (18 out of 30) turned non-anemic, where as 23.33% of the patients (7 out of 30) gotmoderate results, and 16.66% of the patients. (5 out of 30) did not respond much to thetreatment. 16 14 12 10
    • Pravara Madhyama AvaraTable No.9: RBC levels before treatmentRBC levels Males Females Total PercentagePravara 0 0 0 0Madhyama 2 11 13 43.33Avara 3 14 17 56.66The 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 are43.33% (13 out of 30). 14 12 10 8 M a le F e m a le 6 4 2 0 P ra va ra M adhyam a A va ra
    • 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 30The R.B.C. levels showed gradually increase with in 21 days from the starging day oftreatment. The Avara group of patients before the treatment decreased from 56.66% to13.3%. TABLE NO: 11RBC levels after 45 days of treatmentRBC levels Males Females Total Percentage Pravara 3 11 14 46.7 Madhyama 2 9 11 36.6 Avara 0 5 5 16.66RBC levels showed best results after 45 days from the starting day of treatment. TheAvara group of patients with very low RBC levels before the treatment decreasedfrom 30% to 16.66%, Madhyama group of patients decreased to 56.66% to 36.6% andPravara group of patients increased to 13.33% to 46.7% with the increase in RBClevels. 12 10
    • Table No. 13: Final Result After Completion of ResultResults Males Females Total PercentagePravana 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 patientsfelt comfortable. 16 14 12 10 Male 8 Female 6 4
    • Responced based on After Completion of Treatment Male Female6.6%3.3% 13.3% 6.6% 53.33% Pravara Pravara Madhyama Madhyama Avara 16.6% Avara 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 is0.8, 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 is0.6, SE is 0.11, t is 1.3 and p is <0.1.
    • DISCUSSION Pandu roga is one of the most common disease described in Ayurveda. Thedetailed description about it in all aspect is available in most of the Ayurvedicclassics. It is a highly prevalent disease. Ayurveda offers a number of effectiveformulations in the management of pandu roga. The compound drug "Bhaskara lavanachurna" with takra has been selected for the clinical trial to prove its efficacy inraktalpatha 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 aremore prone disorder. So the present clinic trial is conducted to find out an effectivetreatment for anaemia.
    • The etiological factors of pandu roga found in Ayurveda can be studied under 4groups Ahara, Vihara, Manasika, and nidanurthakara Rogas, due to the excessiveintake and practice of above factors. The disease pandu is manifested due to the predominance of pitta in thepathogenisis of the disease, though vatadi tridoshas are vitiated in the samprapti. Theconsumed food, which has the proparties of kshara, amla, lavana, ati ushna etc, acts aspredisposing 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 formsand 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 scienceare comparable with raktalpata condition of pandu roga. The compound drug i.e. "Bhaskara lavana choornam has been selected. for thisstudy 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 areconsidered for their effective management of Pandu roga.
    • The Dadima, pippali, pappli mula, Dhanyaka, jeeraka, Tejo pathra and Twakcontains the property of krimigna. So are responsible for the elimination of worminfestation, which is the one of the cause of the pandu roga. The Balya property of swethajeeraka assists in alleviating the dhatukshya andojokshaya, present in Pandu Roga. The statement "Samanyam Ekatwa karam" mentioned in ayurvedic classics isjustified by asrik prasadana propperty of Dadima, Shunti, Jeeraka in pandu roga. Takram, which is used as anupana in the clinical trial, is Tridoshashamaka andagnideepana. It can also prevent dhamani pratichaya because it is srotho sodhaka aswell as vatahara drarvya. The gradual increase in the Hb levels is observed with in the first weak oftreatment and it reaches the maximum levels in 45 days of duration. This may increasein Hemoglobin levels is attributed to increased production of intrinsic factors byBhaskara lavana churnam. The increased production of intrinsic factor alsocontributes to the increased up take of lohamsa in ahara and oushadha. Improvementin 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 agnideepana and pachana proparties. In two pateints, purgation is noticed on the first two days of tretment. This wasthought as adverse effect noticed during the study. It got relieved after adjustment ofthe 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 completelyachieved by the end of the treatment.
    • The increased production of intrinsic factors also contributes to the increaseduptake 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 antiinflamatery, antiseptic and anodyne properties of Bhaskaralavan churnam. Thus the reduced rakta in the body is agian replanished by the treatment withBhaskara lavana churnam . The conditions of the patients before and after treatment are assessed based onthe parameters (both subjective and objective). The patients are followed up for 45days 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 clinicalpicture and laboratory investigation. The prevelence of pandu roga according to present study found more in females83.33%, (25 out of 30). Than the males 16.66% . Among these cases (7 out of 25) females were suffering with Desfunctionaluterine 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 oftreatment. 56.66% Non-vegetarians got better results than that of vegetarians according todiet.
    • 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, becausemalnutritional diet, irregular food habits. In these leads to anaemia. After thetreatment 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 drugsPippali, Mareecha, Shunti, Amlavetasa, Jeeraka, Tejoptra and Talisa patra ofBhaskaralavana 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 discussedelaborately under respective heading. The results are analysed statistically andconclusions are drawn. CONCLUSION The 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 used routienly in the management of pandu especially on mass level as it works out 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/HOSPITAL ERRAGADDA, HYDERABAD – 500038 DEPARTMENT OF KAYA CHIKITSA – P.G. UNIT SPECIAL CASE SHEETON PANDU ROGAName 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 EXAMINATION a) 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) TemperatureROGI PAREEKSHA: 1. SHADVIDHA PAREEKSHA 1) Prakriti: Vata/Pitta/kapha 2) Vikriti: Dosha – vata / pitta / kapha Dooshya – Rasa / Rakta / mamsa / medo/Asthi/majja/sukra 3) Sara: Pravara / Madhyama / Avara 4) Satwa: Pravara / Madhyama / Avara 5) Samhanana: Susamhana / Madhyama / Asamhana 6) Pramana: Pravara / Madhayama / Avara 7) Satmya: Pravara / Madhyama / Avara 8) Aharashakti: Abhyavaharana shakti – Pravara / Madhyama / Avara Jarana – Pravara / Madhyama / Avara Jatharagni – Pravara / Madhyama / Avara
    • 9) Vayah: Bala/ Yavana / Sampoornatha / Parihari / Vriddha. 10) Vyoyama shakti: Pravara / Madhyama / Avara Desha – Jangala / Anupa / Sadharana Kala – Seetha / Ushna/ Varsha 2. ASHTASTHANA PAREEKSHA:1. Nadi: Vata/ Pitta/ Kapha/ Dwandaja / Sannipataja. Sankhya - /min. Gati – kshipra / manda2. Mala: Varna – Peelha / swetha / Prakrita Sama / Nirama / Vibandha. Pravritti: Adika / Prakrita/ Alpa3. Mootra: Varna – Peeta / Swetha / Prakrita Pravritti – Adhika / Prakriti / Alpa Pramana – Adhika / Prakrita / Alpa4. Jihwa: Amayukta/ Niramayukta5. Twak: Varnam – Pandu / Peeta / Rakta / Ruksha / Snigda6. Shabda: Karnaksweda / Shabda asahana / Prakrita7. Drik: Harswa drishti / Deerga drishti Netravarnam – Swetha / Peeta / Atipeeta / Ruksha / Snigda8. Akriti: Ksheena / Sthoola / Madhyama Sodha – Mukha / Hasta / PadaSROTHAS 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) a) Peethatwam a) Suklatwam a) SothaRukshatwa (yellowishness) (Whiteness) (Swelling)(paleness & Mala Twak AkshikutaDryness) Mutra Mutra BruTwak Mutra Nakha Jihwa MedraNetra Nakha Jihwa Nakha GudaJihwa Twak Netra Yonib) Toda(Priking d) Daha b) Swayathu b) Rakta,Senstion) (burning (Swelling) Kaphamisrita sensation) ,
    • c)Kampa Vamana(Tremours) c) trishna c) Tandra (Diarrhoea) (Thirsty) (Drousiness)d) Anaha(Distension) d) Jwara d) Alasya (Fever) (Slugishness)e) Branma(giddiness) e) Bhinnavit/ e) Atigourava Atisara (Heavyness)f) Swasa(Shortness f) Aruchiof breath) (Dysphasia)g) Dourbalya(debility) Nutritional Infection Endocrine Drugs Worm infestion Bleeding disorders Genetic disordersS.No. Ist day 21st day 45th day1 CBP: Hb% RBC2 ESR3 Stool examination4 Urinary analysis5 Ultra sound abdomen6 Chest X-ray7 OthersVYADHI VINISCHAYA:TREATMENT UNDERTAKEN a) Drug prescribed b) Dosage schedule c) Duration of treatment givenFINAL CONCLUSION a) Cure in percentage b) Response to treatment c) Special not if any
    • RESULT a) Pravara b) Madhyama c) AvaraSign. Of the Co-guide Sign. Of the Guide Sign. Of the PG.Scholar INFORMED CONSENT I, ................................... Son/ daughter / wife of ................................. amexercising my free will to participate in above study as a subject. I have been informedto my satisfaction by the attending physician the purpose of clinical evaluatin and thenature of the drug-treatment. I am also aware of my right to opt out of the treatmentschedule at any time during the course of the treatment.Schedule initiation Patient Signature BIBLIOGRAPHYS.No. Name of the Book Authors Name Publication1. Amarakosha Amara simha Choukambha Sanskrit2 A.P.I. Textbook Hon. Brig. K.K. Association of Physicians of medicine,II Vol Datey S.E.M. of India, Bombay, 19793 Astanga Hridaya V. Ramaswamy Telugu, Academy, Hyderabad 1979
    • 4 Astanga Sangraha V. Rangacharyulu Vavilla press, Madras 19545 Astanga Sangraha Puryanchlok Sri Swati enterprises, Pandit Lalchandra Nagpur,6 A Text Book of William Byoid 9th Edition, 1990 Pathology7 A Text Book of N. Murgesh Satya Publishers, Pharmacology Madhurai, 4th Edition 19978 Basavarajeeyam P. Satyanarayana Konda Sankaraiah Book Rao Depot, Secunderabad9 Bhaishajya Ambika Datta Choukambha Sanskrit Ratnavali Sastry Samsthan, Varanasi, 198110. Bhava prakasha Mukkamala Sri Panduranga printing Venkata Sastry works, Vijayawada, 2nd Edition, 195911. Bhava prakasha Dr. Krishnachandra Choukamba Sanskrit Nighantu Chunekar Samsthan, Varanasi 5th Edition, 195912 Bhela Samhita S.V.S. Shastry CCRIM & H, C.R.R. Sharma New Delhi, 197713 Chakradatta Sri Jagadeshwar Choukamba Sanskrit Prasada Tirupathi Samsthan, Varanasi14 Charaka Samhita Sripada Krishna Sunrise printers, Rajah- Moorthy Shastry mundry, 4th Edition, 198915 Charaka Samhita Agnivesha V. Ramaswamy & Sons, Madras16 Clinical Medicine Praveen Kumar ELBS with Balliere, Michael Clark Tindall, 3rd Edition, 199417 Clinical Methods Michael Swash ELBS series, Govt. of UK18 Clinical Hematology Wintrobb M.M. 5th Edition19 Clinical Methods Prof. K.R. Srikanta Choukamba Orientalia, in Ayurveda Moorthy Varanasi, 1st Edition 1983
    • 20 Current Medical Steven A. Schroeds Lange Medical Books, Diagnosis and USA Treatment21 Digestion and C. Dwarakanath Baidyanath Ayurved Metabolism Bhavan Pvt. Ltd. Calcutta 1st Edition22 Dravvyaguna K. Nishteshwar AP Ayur. Literature Improvement trust, Hyderabad23 Effect of Hormones Cannady 1962 in anaemia24 Essentials of Medical K.D. Tripathi Japee Brothers Medical Pharmacology publishers, PVT Ltd., New, Delhi, 199925. Haritha Samhita Khemaraj Sri Sri Vangeshwara Krishnadas Mudranalaya, 198426. How to examine a Dr. Menino de Varghese Publishing Patient Souza House, Bombay 1982, 5th Edition27 Human Physiology C.C. Chaterjee Medical allied agency, Culcutta, 11th Edition,198828 Human Physiology Chakrabarthi The New Book Stall, H.N. Ghosh Calcutta29 Human Physiology Arthur C. Guyton Prism Books Pvt. Ltd. John E. Hall 9th Edition, 199630 Immunological Capplan 1963 Studies in Anemia31 Indian Medicinal KR. Kirtikar Jayyed Press, Delhi Plants B.D. Basu 2nd Edition, 197532 Indian Medicinal Orient Longman Ayurvaidhyasala, Plants Kottakal33 Introduction to C.Dwarakanath Choukamba Orientalia,
    • Kayachikitsa Varanasi, 2nd Ediction198634 Kashyapa samhita Pandit Hemaraj Choukamba Sanskrit series, Varanasi35 Madhava Nidana M.Vishweshwar Nirnaya sagar Press, Bombay, 195836 Medicine for Dr. K. Choudary Jaypee Brothers Medical Students and Practitioners Publishers, New Delhi 199037 Nighantu Adarsha Bapalal G.Vaidya Choukamba Bharati Academy, Varanasi38 Pharmacology R.S.Satoskar & Popular Prakashan Pvt. Bhandarkar Ltd. Bombay39 Principles & Practic Davidson 1962 of Medicine40 Principles of Anatomy Gerard J. Harper & Row Tortora publications, New york, 198441 Principles of Harrison 12th Edition, 1991 of Internal Medicine42. Shabdarnavam - -43. Shabda Raja Radhakant Vyaptistamisana Press, Kalpadruvam Dev Bahadur Culcutta, 180844. Shabda ratnavali - -45. Shabdasthoma Sri taranath Veedanyantra PRess, Mahanidhi Takravachaspathi Calcutta, 197646. Sarangadhara Sarangadhara V. Ramaswami Sastrulu Samhita Mishra & Sons, Vavilla Press, Madras, 1952.47. Susruta Samhita V. Ramaswami Vavilla press, Madras
    • Shastrulu 195448 Susruta Samhita Ambikadatta Choukambha Samsthan, Sastry Varanasi, 4th Edition 197949 The Indian Materia Dr. K.M. Nadkarni Popular Book Depot, Medica Bombay.50 The Iron Deficiency Gibbson 1963 & Pernicious Anaemia51. The Wealth of CSIR, New Delhi, 1969 India, Vol, III, VIII & IX52. Vaidhya Chintamani Indrakanti Venkateshwara Book Vallabhacharyulu Depot. Secbad. 195553. 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